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PHD > Final > Flashcards

Final Flashcards

1
Q

Which medication causes peripheral neuropathy as a side effect?

A

Patients taking isoniazid, which can inhibit enzymes required for vitamin B6 production, can develop peripheral neuropathy due to demyelination.

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2
Q

Side effect of ethambutol

A

optic neuropathy

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3
Q

Nitrite positive indicates what type of gram bacteria?

A 
Gram negative (proteus, e coli) 
Rule out staph sapro and enterococcus

Uti

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4
Q

Type of bacteria N. meningitis

A

gram negative diplococci

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5
Q

What type of stain for legionnaires? How does it spread?

A

Use silver stain for legionnaires, rod shaped. Dullness to percussion indicates “pleural effusion.” Spread via water droplets from contaminated water systems, hot water tanks, air conditioning. Nursing homes, cruise ships

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6
Q

Stain for chlamydia

A

Giemsa stain for Chlamydia

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7
Q

Stain for Crytococcus neoformans

A

India Ink for Crytococcus neoformans

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8
Q

Mycobacteria staining

A

Ziehl-Neelson mycobacteria

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9
Q

Pneumocystis jiroveci stain

A

Gomoro methenamine silver stain for pneumocystic jiroveci.

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10
Q

What stains silver?

A

Silver Stain: HeLiCoPters Are silver -> Helicobacter pylori, Legionella, Bartonella henselae, Coccidoises, Pneumocystic jirovecii, Aspergiullus)

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11
Q

What do you find in CSF findings of N meningitidits? What are normal glucose, protein, opening pressure levels? What’s the most common cause of meningitis in neonates?

A

You’ll find increased PMN, increased protein, and decreased glucose. Normal glucose is 40-70 ish, normal protein is <40. Normal opening pressure 70-180. Neutrophils dominant. E Coli is common cause of meningitis in neonates

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12
Q

Poor oral hygiene and abscesses in buccal mucosa is indicative of:

A

actinomyces israellii. Causes oral/facial abscesses that drain through sinus tracts, associated w dental caries, normally in mouth, colon, vagina

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13
Q

What causes peptic ulcers? And how?

A

Common cause of peptic ulcer disease is H pylori infection, causes mucosal damage through production of ammonia, neutralizes stomach acid and increases pH of the environment, flagella present help them migrate toward gastric epithelium.

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14
Q

H. Pylori is a triple threat. What does that mean?

A

It’s triple positive, catalase, oxidase, and urease positive. Urease most important for neutralizing stomach acid. It also requires 3 drugs - amoxicillin, clarithromycin, proton pump inhibitor (antibiotics cure pylori)

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15
Q

What is the use of bronchoalveolar lavage? It’s usually determines which pathogens?

A

Bronchoalveolar lavage: Used when suspecting an infectious etiology in patients who are unable to expectorate sputum for examination (e.g., tuberculosis, PCP, histoplasmosis, aspergillosis);

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16
Q

What’s imipenem’s MOA?

A

Imipenem is a broad-spectrum antiobiotic from the carbapenem class. It’s coadministered with cilastatin, an inhibitor of renal drug metabolism– so effective serum levels of imipenem can be maintained and nephrotoxicity is prevented. Impenem broad spectrum, beta lactamase resistant carbapenem- binds penicillin-binding proteins and inhibits cell wall synthesis. ALWAYS administered with cilastatin

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17
Q

When do you administer cilastatin?

A

With impenem- cilastatin is an inhibitor of renal drug metabolism– so effective serum levels of imipenem can be maintained and nephrotoxicity is prevented.

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18
Q

Virulence factors for Hemophilia Influenzae

A

Septic arthritis - presents with fever and acute monoarticular joint paint. HiB only affects children who haven’t had the vaccine.

Contains virulent capsule.

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19
Q

Protein A is found in… and is…

A

-Cell wall protein that binds human IgG -> protein A -> Staph aureus `

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20
Q

Brucella is common in…what population?

A

Brucella- undulant fever, night sweats, arthalgia, anorexia– unpasteurized milk. Dairy farmers or animal farmers or veteraniarians or those who consume unpasteurized dairy products.

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21
Q

Symptoms of brucella

A

Brucella- undulant fever, night sweats, arthalgia, anorexia– unpasteurized milk.

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22
Q

How is bartonella henselae transmitted?

A

Bartonella henselae transmitted via cat scratch and results in lesion,

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23
Q

Pasteurella multocida is transmitted how?

A

Pasteurella multocida acquired via cat or dog bite

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24
Q

Virulence factor of Klebsiella

A

Klebsiella is a gram NEGATIVE rod. Virulence factor: capsular polysaccharide for antiphagocytic effect;

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25
Q

Exotoxin A is a virulence factor of what?

A

Exotoxin A -> Psueudomonas -> associated with green colored sputum because of pyocyanin and pyoverdin;

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26
Q

IgA protease virulence factor of what?

A

IgA protease virulence factor of H. influenzae and Strep pneumo (can cause lung abscess);

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27
Q

P fimbriae virulence factor of what?

A

P-fimbriae: E coli;

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28
Q

K capsule virulence factor of what? Causes what?

A

K capsule-E coli pneumonia

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29
Q

What’s an endotoxin found on outer membrane of gram-negative bacteria?

A

Lipooligosaccharide expression

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30
Q

What’s the primary virulence factor in meningococcemia?

A

Lipooligosaccharide expression

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31
Q

Streptococcal Toxic shock syndrome is caused by what toxin and what pathogen?

A

Erythrogenic toxin from Streptococcus pyogenes- GAS. Follows cutaneous infection (impetigo) and isn’t associated with tampon use

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32
Q

What causes TSS, and what is its mechanism?

A

Tampon use; Toxic shock syndrome caused by bacterial exotoxins, TSST-1 produced by Staph aureus- superantigen that triggers polyclonal T cell activation. Results in massive release of IL-2, IFN-gamma, and TNF alpha. Oropharyngeal hperemia and diffuse macular erythroderma.

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33
Q

Peptostreptococcus is _ hemolytic, coag ?, and appears in clusters or chains?

A

Peptostreptococcus is gamma hemolytic, coag negative, and appear in chains. Lung abscess, found in oral cavity.

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34
Q

IgA protease is a virulence factor for: (3)

A

IgA protease: S pneumoniae, H influenzae, Neisseria

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35
Q

M protein is a virulence factor in:

A

M protein is found in GAS, strep pyogenes. Coag negative, gram positive.

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36
Q

Lethal factor virulence factor in:

A

Lethal factor -> Bac anthracis

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37
Q

Staph aureus virulence factor:

A

Staph aureus is a beta hemolytic, coagulase-positive cocci in clusters. Staph A. virulence factor is protein A, which impairs phagocytosis and opsonization of bacteria by binding the Fc region of IgG.

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38
Q

Phosphlipase C, virulence factor in: (4)

A

Phosphlipase C, virulence factor in Pseudomonas aeruginosa, Clostridum spp., Listeria, Myo TB

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39
Q

Tpa meds end with what suffix? What’s the timing that you administer it?

A

Thrombolytics (i.e. activators of tpa) include meds that ends with -PLASE. (Alteplase, reteplase, streptokinase, tenecteplase). They convert plasminogen to plasmin, which degrades fibrin and lyses formed clots. Given within 4.5 hours of symptom onset.

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40
Q

What’s the effect of warfarin?

A

Warfarin is used in chronic setting, not acute- vitamin K antagonist used for prophylaxis of ischemic stroke. Inhibits hepatic epoxide reducatse -> 2, 7, 9, 10, C, S affected.

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41
Q

What is the effect of heparin?

A

Heparin used for acute treatment of thromboembolism, pulm embolism- activates antithrombin III and will inhibit thrombin and factor X. Not helpful to use in acute ischemic stroke. Helpful for prophylaxis in venous thrombosis.

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42
Q

Gamma carboxylation needs what and activates what?

A

Gamma carboxylation activates factors 2, 7, 9, 10, C, S via vitamin K and happens in the liver. Chronic alcohol abuse would affect the liver’s function causing vit K deficiency, poor nutrition, etc.

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43
Q

What does Protein S + Protein C complex inhibit?

A

Protein S + Protein C complex inhibits Factors VIII and V, causing hypercoagulation state.

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44
Q

Manifestation of labs for von willebrand, manifestations clinically?

A

Von willebrand deficiency would only manifest as mild bleeding, maniefests with prolonged bleeding time, normal PT, normal or prolonged PTT.

epistaxis, gingival bleeding, and/or menorrhagia.

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45
Q

What is one really terrible side effect of tPA?

A

Thrombolytic therapy- tPA can lead to intracerebral hemorrhage as a side effect. Contraindications of tPA: bleeding, recent surgery.

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46
Q

Name two meds that can reverse effects of tPA.

A

Antifibrinolytics such as aminocaproic acid and tranexamic acid can reverse the effects of tissue plasminogen activators by inhibiting the activation of plasminogen

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47
Q

-Impaired platelet adhesion due to a defect in the glycoprotein Ib receptor results in what?

A

-Impaired platelet adhesion due to a defect in the glycoprotein Ib receptor (the primary von Willebrand factor receptor) results in Bernard-Soulier disease. Laboratory testing usually reveals thrombocytopenia and prolonged bleeding time, but the partial thromboplastin time is normal.

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48
Q

What does tissue factor expression on inflammatory cells indicate?

A

-Tissue factor expression on inflammatory cells describes the activation of the coagulation cascade and thrombocytopenia seen in disseminated intravascular coagulation (DIC).

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49
Q

Blastomycosis “buzz words”: location, replication, finding

A

Eastern and Central US, Great Lakes, “Broad based budding”, Verrucous lesions

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50
Q

Histoplasma “buzz words”, location, histology, associated with..

A

Hisplasma -> Mississipi and Ohio River Valley, macrophages filled with histoplasma, bat/bird droppings/caves

51
Q

Histologic findings in aspergillus:

A

-Aspergillus infection is seen in immunocompromised patients, or in those with asthma or cystic fibrosis (allergic bronchopulmonary aspergillosis). Histologic findings would include branching hyphae with septae.

52
Q

What shows up as thrush? What organ does this organism usually affect? What do you see in histology?

A

-Candida albicans is the cause of thrush and is seen most often in immunocompromised patients, such as those with HIV infection. Candida infection, however, is more likely to affect the esophagus than the airways and lungs. In a tissue biopsy specimen, it will be seen as pseudohyphae and budding yeast.

53
Q

Coccidioidmycosis buzz words

A

Coccidioidomycosis-> Southwestern US, AZ, CA, earthquakes, dust -> spherule filled endospores, meningitis

54
Q

Paracoccidioidomycosis buzz words, location and histology

A

Latin America, “Captain’s wheel formation”

55
Q

KOH shows what in candida infections?

A

If KOH shows hyphae and pseudohyphae, it’s candida. Will present with skin problems. Usually affects immunocompromised - HIV/ diabetes.

56
Q

Cellulitis is associated with what pathogens?

A

Cellulitis associated with staph aureus or strep pyogenes.

57
Q

KOH showing branching, septate hyphae indicates what?

A

tinea- cutaneous fungus

58
Q

Vaginalis candidiasis - pH? associated with?

A

pH normal, around 3.85-4.5; associated with antibiotics, contraceptives, and diabetes, “cottage cheese” discharge

59
Q

Trichomonas - pH? Discharge?

A

-Trichomonas vaginalis, pH around 5-7, frothy, yellow- green vaginal discharge like a spinach smoothie

60
Q

Stand out side effect of protease inhibitors (-navir)

A

Redistribution of fat is commonly caused by protease inhibitors (-navir); lipodystrophy

61
Q

Stand out side effect of integrate inhibitors (-tegravir)

A

-Integratase inhibitors for HIV -> increased creatine kinase

62
Q

MOA nystatin? Used to treat…

A

Nystatin functions by binding to ergosterol (the sterol specific to fungal cell membranes), forming pores and disrupting the fungal cell membrane.

-treats oral thrush, first line of treatment

63
Q

Germ tube positive means…

A

candida! @37 degrees

64
Q

Pseudomonas virulence factor

A

Virulence factor for pseudomonas: PEEP: Phospholipase C, Endotoxin (fever, shock), exotoxin A, pigments (pyoverdin, pyocyanine)

65
Q

Staph aureus virulence

A

-Staph aureus- Protein A virulence

66
Q

Staph pyo virulence

A

-Staph pyogenes- M protein, strepsolysin O, Streptokinase, DNAses virulence factors

67
Q

Clostridium dificile virulence

A

-Clostridium dificile- toxin B

68
Q

alpha toxin is virulence factor for

A

-Clostridium perfringens- alpha toxin

69
Q

Dental caries associated with…

A

strep viridans

70
Q

Colon cancer associated with…

A

Strep bovis

71
Q

dry cough, prisons/military recruits, lesions on extensor surfaces

A

mycoplasma

72
Q

HiB most invasive strain because…?

A

due to polyribosylribitol capsule that inhibits complement mediated phagocytosis. Can use a conjugated vaccine for this. Nontypeable type of influenza not covered by vaccine. Hib leads to meningitis

73
Q

Infective endocarditis can be caused by which pathogens, how, and manifests as what? (5)

A

Infective endocarditis can be caused by staph aureus (IV drug use), staph epidermis (heart valve/ prosthetics), enterococci (post GU/GI procedures), staph gallolyticus (associated w colon cancer), strep viridans (dental caries). Clinically manifests: mumurs, Osler nodes on pads of fingers.

74
Q

Cornybacterium diptheriae A, B, C, D, E: gimme!

A 
-Cornybacterium diphtheriae:
A: ADP ribosylation
B: Beta prophage
C: Cornybacterium
D: Diphtheriae
E: Elongation Factor 2
-Pseudomembranous pharingitis with lymphadenopathy "bull's neck appearance"
75
Q

Vancomycin MOA? Clinical use? Resistance?

A

inhibits cell wall peptidoglycan formation by DIRECTLY binding D-ala-D-Ala portion. Treats gram positive drugs. ONLY. The big dog. Resistance happens when bacteria change from D-ala-D-Ala to D-ala-D-LAC. Not sensitive to beta lactamases

76
Q

Penicillin MOA? Clinical use?

A

Penicillin is also a D-Ala-D-Ala analog, but it binds transpeptidases and blocks the cross-linking of peptidoglycan cell wall. Used for gram +, gram - (N meningitidis) and syphillis.

77
Q

Peptidoglycan is made up of what precursors?

A

disaccharide composed of N-acetylmuramic acid (MurNAc) and N-acetylglucosamine (GlcNAc

78
Q

Describe how necator americanus and ancylostoma duodenale invade. What are the signs?

A

Hookworm eggs get laid in soil, they come in contact with human skin (walking barefoot) and get transmitted that way. They travel up to the lung and then get coughed up and swallowed, where they go to GI. In the small intestine, the larvae mature into adults, attach to the gastrointestinal mucosa, and feed on human blood by lacerating capillaries. Biggest risk of hookworm infection is iron-deficiency anemia (microcytic anemia) due to chronic blood loss. “thin walled” eggs. Eosinophilia important dx clue too

79
Q

What is Chagas disease linked to, and what is it caused by?

A

-Chagas disease is linked to dilated cardiomyopathy and is most common in Latin America. It is caused by the protozoa Trypanosoma cruzi. Transmission occurs during a triatomine bug bite.

80
Q

Cystic fibrosis susceptible to which infectious pathogens?

A

Recurrent sinopulmonary infections (eg, Staphylococcus aureus, Pseudomonas aeruginosa, & Burkholderia cepacia complex - progression)

81
Q

Streptoccus should be plated on…

A

Should be plated on: regular blood (eg, Streptococcus),

82
Q

Chocolate agar for…

A

chocolate (eg, H influenzae)

83
Q

MacConkey agar for…

A

and MacConkey (eg, Pseudomonas) agars

84
Q

S aureus plated on…

A

sputum should also be plated on mannitol salt agar (eg,S aureus

85
Q

Segmented viruses are: (how many segments?)

A

Bunyavirus: 3 segments
Orthomyxovirus: 8 segments
Arenavirus: 2 segments
Reovirus: 10–12 segments

86
Q

Which virus is naked and single stranded DNA?

A

Parvovirus B19 is one of the few nonenveloped ssDNA viruses that infect humans. It can lead to transplacental fetal infection.

All are dsDNA except “part of a virus” parvo.

87
Q

The TORCHHeS infections are:

A 
Toxoplasmosis
Others (varicella, parvovirus B19 infection, listeriosis)-VPL 
Rubella
Cytomegaly (CMV)
Herpes simplex virus (HSV) infection
HIV 
Syphilis
88
Q

Negative stranded RNA virus

A

They include arenaviruses, bunyaviruses, paramyxoviruses, orthomyxoviruses, filoviruses, and rhabdoviruses.

Always Bring Polymerase Or Fail Replication

89
Q

Positive Sense RNA

A

I went to a retro (retrovirus) toga (togavirus) party, where
I drank flavored (flavivirus) Corona (coronavirus) and ate hippie (hepevirus) California (calicivirus) pickles (picornavirus).

90
Q

Which one is a double stranded RNA?

A

Reovirus - RepeatO virus

91
Q

DNA Viruses are…

A 
Hepadnavirus
Herpesvirus (8) 
Adenovirus
Pox
Parvovirus
Polyoma
Papilloma 
Y
92
Q

Genetic recombination/reassortment occurs in…

A

The observed exchange of entire RNA segments is an example of reassortment, which can only occur in viruses with segmented genomes

BOAR

93
Q

In ETEC, abdominal cramping, nausea/vomiting, fever, watery diarrhea. What toxin does it resemble?

A

Following ingestion, ETEC colonizes and adheres to small intestine enterocytes (mediated by pili). The typical manifestations of abdominal cramping, nausea/vomiting, and (occasionally) low-grade fever occur due to the elaboration of plasmid-encoded heat-labile (LT) and/or heat-stable (ST) enterotoxins:

The LT enterotoxin, which resembles cholera toxin in structure and mode of action, increases cyclic AMP in gut mucosal cells by activating adenylate cyclase.

The ST enterotoxin (which is not inactivated by heat likely due to its small molecular size)causes an increase in cyclic GMP by activating guanylate cyclase.

Both mechanisms result in increased chloride secretion and decreased sodium reabsorption by enterocytes, resulting inwatery diarrhea.

94
Q

Endotoxin is found in what bacteria? What is the inflammatory response?

A

Endotoxin is a lipopolysaccharide found in the cell membrane of gram-negative bacteria. When released into the bloodstream, endotoxin causes a severe inflammatory response (eg, fever, hypotension) mediated by TNF-alpha and IL-1 secreted from activated macrophages. However, endotoxin is present at high concentrations in the normal gut microbiota and does not cause gastrointestinal illness.

95
Q

How does Hep B replicate?

A

The hepatitis B virus (HBV) replicates via the following sequence: double-stranded DNA → +RNA template → partially double-stranded DNA progeny.

96
Q

Watery diarrhea can be caused by:

A 
ETEC; 
cholera 
Norovirus 
Cryptosporidum
C. Diff
Rotavirus (unlikely in vaccinated children)
97
Q

Bloody stools:

A

Campylobacter jejuni
E coli
Shigella (watery to bloody)

98
Q

Where does parvovirus replicate?

A

Parvovirus B19 replicates in erythrocyte precursors in the bone marrow. These cells express blood group P antigen (also known as globoside), which is the cellular receptor for parvovirus B19. Viral replication in the nucleus leads to cell lysis (ie, decreased reticulocytes and red blood cells). Acute and chronic sequelae of parvovirus B19 infection can occur in specific populations (eg, chronic anemia in immunosuppressed patients, aplastic crisis in those with underlying hematologic abnormalities such as sickle cell disease).

99
Q

What is recommended in patients with measles?

A

Acute measles infection depletes vitamin A stores, resulting in a risk of keratitis and corneal ulceration. Vitamin A helps prevent and treat these ocular complications. In addition, it reduces risk of other comorbidities (eg, pneumonia, encephalitis), recovery time, and length of hospital stay. No other vitamin is linked to measles.

100
Q

Sympoms of Francisella

A

The symptoms of tularemia are dependent on the route of transmission. Ulceroglandular disease, the most common presentation, typically occurs after cutaneous inoculation. Patients develop a single papuloulcerative lesion with surrounding erythema and a central eschar at the site of transmission. Tender regional lymphadenopathy occurs simultaneously or within a few days and may become suppurative. Most patients have fever. Sometimes, the cutaneous lesion is not present; other forms of tularemia can also occur, including pneumonia

101
Q

Two key manifestations of malaria. What’s seen on histology?

A

Manifestations of malaria arise due to erythrocyte rupture and include fever, flu-like symptoms (eg, myalgia, fatigue, headache, chills), ANEMIA, and INDIRECT BILIRUBINEMIA (hepatosplenomegaly is also common). The diagnosis is confirmed when trophozoites (intraerythrocytic, ringed inclusions) are seen on peripheral blood smear using Giemsa stain.

102
Q

Plasmodium vivax needs to be treated with:

A

Although many different Plasmodium species cause malaria, the 2 dominant organisms are P falciparum (in Africa) and P vivax (in non-African countries). This patient who traveled to India was likely infected with P vivax. Unlike P falciparum, P vivax (and P ovale) sporozoites can undergo a dormant hepatic phase (hypnozoite stage) that may cause recurrent parasitemia and symptoms weeks or months after initial infection. Individuals with these strains of malaria must be treated with a combination of drugs that target both the erythrocyte phase (eg, chloroquine) and the dormant hepatic phase (ie, primaquine) to ensure clearance.

103
Q

What is the tissue tropism of viruses caused by? (i.e. influenza)

A

The tissue tropism of viruses is primarily mediated by viral surface glycoproteins that bind to specific host cell receptors. Mutations to viral surface glycoproteins can alter tissue tropism and cause noninfective viruses to become infectious.

Influenza’s tropism is HA.

104
Q

Which two bacteria form spores?

A

Spore-forming bacteria can survive boiling temperatures. Bacillusand Clostridium species are common pathogenic spore-forming bacteria.

105
Q

Which malaria has a dormant phase?

A

P ovale and P vivax have a dormant hepatic phase (hypnozoite) that may reactivate several months after return from an endemic region (if not treated with primaquine). In contrast, P falciparum does not have a dormant hepatic phase; it matures in (and is released from) the liver over 8-30 days.

106
Q

What does mefloquine do?

A

Mefloquine is a schizonticide that actively destroys replicating parasites within red blood cells. However, it is inactivated in the liver and has no efficacy against hepatic schizonts. Therefore, patients must receive mefloquine chemoprophylaxis for 4 weeks upon return to ensure that parasites released from the liver are destroyed when they infect red blood cells (liver schizonts rupture over 8-30 days).

107
Q

Which organisms cleaves IgA?

A

Streptococcus pneumoniae and Neisseria gonorrhoeae produce IgA proteases that cause cleavage of IgA antibodies, preventing them from interfering with bacterial adhesion to mucous membranes.

108
Q

What are the clinical indications in a mucormycosis infection?

A

Facial pain, headache, and nasal eschar in a patient with likely diabetic ketoacidosis (pH 7.1, positive ketones, and dry mucous membranes in a young patient with recent unintended weight loss) are highly suggestive of mucormycosis. Most cases are rhinocerebral.
Penetrates cribriform plate and enters brain.

109
Q

Buzz words for mucormycosis

A

Patients with DKA or neutropneia, “black necrotic exchar on face”

irregular broad nonseptate ginger hyphae branching at wide angles

110
Q

How does Shigella cause infection?

A

Mucosal invasion is the essential pathogenic mechanism for Shigella infection. Shigella invades the gastrointestinal mucosa, particularly via the M cells that overlie Peyer’s patches (Salmonella does this too). After cell entry, Shigella is able to lyse its containment vacuole and enter the cytosolic compartment. It then can induce apoptosis of the host cell and spread to adjacent cells via protrusions created through host-cell actin polymerization. Shigella invasion triggers a robust host inflammatory response that is largely mediated by neutrophils.

111
Q

Difference btwn shigella and salmonella

A

Shigella doesn’t produce H2S, salmonella does.

112
Q

The 4 F’s of shigella

A

Fingers, Flies, food, feces

113
Q

Population Shigellosis affects

A

primarily peds, MSM, and nursing homes

114
Q

Shiga toxin is produced by:

A

Cytotoxin produced by Escherichia coli O157:H7* & Shigella dysenteriae

MOA: inhibits 60S ribosomal subunit, halts protein synthesis; inflammatory diarrhea
EHEC

115
Q

C Diff virulence factors

A

Clostridioides difficile produces toxin A (enterotoxin) and toxin B (cytotoxin). In contrast to Shiga toxin, toxin A primarily initiates an inflammatory response, whereas toxin B depolymerizes actin filaments, causing gastrointestinal mucosal cell death.

116
Q

EHEC most commonly caused by eating…

A

undercooked meat! bbq or burgers!

117
Q

CD8+ T cells would be important for combating which intestinal pathogens?

A

CD8+ T cells are not important in clearing giardiasis; they are more important for combating intracellular intestinal pathogens such as Cryptosporidium parvum and Toxoplasma gondii.

118
Q

CD21 monoclonal antibodies would help:

A

The EBV envelope glycoprotein gp350 binds to CD21 (also known as CR2), the cellular receptor for the C3d complement component. CD21 is normally present on the surface of B cells (CD19-positive cells) and nasopharyngeal epithelial cells. Therefore, exposure to a monoclonal anti-CD21 antibody could interfere with EBV attachment to B cells.

119
Q

Cellulitis caused by:

A

GAS- strep pyogenes

120
Q

Adalimumab is significant in that it’s a…

A

tumor necrosis factor alpha inhibitor

121
Q

Alcohol-based disinfectants are used to kill what type of viruses?

A

Alcohol-based disinfectants kill enveloped viruses (eg, influenza) by dissolving their outer lipid envelope. Nonenveloped viruses are less susceptible to some alcohol-based disinfectants because they have no lipid envelope to target

122
Q

Lipid A is a virulence factor for what and does what?

A

Lipid A and O antigen are components of lipopolysaccharides, which make up the majority of the outer membrane of gram-negative bacteria. Lipid A is a virulence factor that activates macrophages, leading to widespread release of inflammatory cytokines (eg, IL-1, IL-6, tumor necrosis factor-alpha), which in turn causes endothelial injury, increased vascular permeability, and septic shock. The O antigen is on the outer surface and is a variable polysaccharide used to classify gram-negative bacteria.

123
Q

Which organism can synthesize dextrans from glucose? What is the significance of this?

A

Strep viridans

These gram-positive organisms are capable of producing extracellular polysaccharides (dextrans) using sucrose as a substrate.

Dextrans facilitate streptococcal adherence to fibrin. Fibrin and platelets are deposited at sites of endothelial trauma, providing a site for bacterial adherence and colonization during bacteremia. In patients with pre-existing valvular lesions, viridans streptococci can adhere to the affected valve and establish infection leading to endocarditis.

PHD (4 decks)

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