Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Immuno mikro eng > First Pass Miss Exam 3 > Flashcards

First Pass Miss Exam 3 Flashcards

1
Q

What is the major virulence factor of EPEC?

A

Ability to efface the microvilli and sit on actin pedestal, then type 3 secretion system
-> watery diarrhea in infants / children

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is one final bacterium that can release a heat-labile enterotoxin after ingestion?

A

Clostridium perfringens - much like B. cereus diarrheal form, produced in GI tract. From undercooked food

(alpha toxin, disrupts actin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the four non-inflammatory diarrhea causing parasites in immunocompromised?

A
  1. Cryptosporidium
  2. Microsporidia
  3. Cyclospora -> long diarrhea
  4. Isospora

Micro, Iso, Cyclo

-> MIC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What does Hemolytic uremic syndrome cause? Why?

A

Triad:
Anemia
Thrombocytopenia
Acute renal failure

Due to microthrombi forming on damaged endothelium of renal glomeruli

Seen in Shigella and EHEC, basically there is damage to the glomerulus from Shiga-like toxins which causes platelets to aggregate, and platelet clots end up lysing RBCs as they squeeze by.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How does Shigella cause bacillary dysentery? Do they all produce Shigatoxin?

A

Uses local inflammation produced by PMNs to induce more epithelial damage and allowing more invasion by bacteria, although it typically does not cause sepsis.

Only Shigella dysenteriae produces Shigatoxin, which is a cytotoxin killing more intestinal epithelium (like EHEC).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the mechanism of Shiga-toxins?

A

Binds the 60S ribosomal subunit to cause translational arrest. AB toxin as well, binds the Ganglioside GM3 to get in

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the mechanism of diphtheria toxin and what uses it?

A

Diphtheria and similar toxin include:
P. aeruginosa (Exotoxin A)
C. difficile (Exotoxin B, stops protein synthesis and actin polymerization)

Diphtheria toxins binds EF-2 and stops cellular protein synthesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What will be seen in the stool in Shigella?

A

Large numbers of PMNs + mucoid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How can you distinguish EIEC vs Salmonella vs Shigella?

A

Shigella - lac -
EIEC - lac +
Salmonella - lac - and makes black colonies on Hektoen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How are Salmonella bacteremia and enteric fever told apart?

A

Bacteremia - rarely a positive stool culture. Rapid, spiking fever. Develops following gastroenteritis

Typhoid - positive culture only later in disease. Also has an INSIDIOUS onset rather than acute. That is, a slowly rising fever rather than a rapid, spiking fever. Blood diarrhea will occur later.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How is campylobacter identified and cultured?

A

Microaerophilic and capnophilic, grows at campfire temperatures (42 C)

Gram negative curved oxidase positive rod (like Vibrio)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the major difference between Vibrio parahaemolyticus and Vibro cholerae?

A

Although both are transmitted in seafood, only the former is halophilic and causes bloody diarrhea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Other than pet feces, what is one major reservoir for Yersinia enterocolitica?

A

Transfusion-related septicemia -> can grow in blood that is refrigerated.

Causes mesenteric lymphadenitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

In what way is E. histolytica similar in adherence to UPEC’s P-pilus

A

Both bind sugar receptors and are thus sugar-sensitive in the lab

E histolytica = galactose
E. coli = mannose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How is H. pylori identified in the lab?

A

Oxidase positive, campylobacterlike organism, gram negative and curved. Urease positive.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What types of colitis do C. difficile and Shigella cause?

A

C. difficile - pseudomembranous

Shigella - ulcerative

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is a common causative agent of intraperitoneal abscess? How is it identified?

A

Bacteroides fragilis, a gram-negative encapsulated anaerobic bacillus.

Identified via foul-smelling discharge and broad antibiotic resistance (i.e. aminoglycosides because they are oxygen-dependent)

These abscesses are typically polymicrobial (with facultative anaerobes)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are common causes of pancreatic and hepatic abscesses?

A

Pancreatic - peptic ulcers

Hepatic - biliary tract disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What causes splenic abscess?

A

Whatever is seeding a bacterial infection elsewhere in the body

i.e. intraperitoneal = bacteroides
right-sided endocarditis = S. aureus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is diverticulitis?

A

when herniation of mucosa and submucosa ruptures, leads to peritonitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is the most diagnostic thing that shows the presence of a recent HBV infection? What is the critical period which we are covering for?

A

Presence of IgM antibodies to Hepatitis B core antigen (HBcAg)

Will persist even during the window period when HepB surface antigen (HBsAg) is not seen in the blood, and anti-HBsAg are not of protective, detectable titers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the mechanism of formation of mRNA in HBV viral replication cycle within hepatocytes?

A
  1. Enters the cell, is uncoating, and the partially dsDNA is converted into cccDNA (covalently closed circular form DNA) by host enzymes.
  2. Minus strand DNA is transcribed into full length plus-strand RNA by host DNA polymerase 2
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is the function of the P protein in HBV?

A

Uses the full length viral mRNA to Reverse-transcribe to full length (-) sense DNA. Then uses full length (-) DNA to transcribe a partial + strand.

It is a DNA/RNA-dependent DNA polymerase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is delta antigen?

A

The only protein encoded by the - sense ssRNA virus Hepatitis D -> functions in RNA encapsidation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What histological finding is characteristic of acute hepatitis?

A

Councilman bodies - ballooning hepatocytes + dark staining necrotic / apoptotic hepatocytes

Hep A often causes this

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is asterixis?

A

Hand tremor which can accompany the lethargy and stupor associated with fulminant hepatitis (liver failure)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

In terms of labs, what is the difference between Chronic Hepatitis B and Carrier Hep B?

A

In chronic hep B, liver enzyme tests will be abnormal, but they are normal in carrier hep. HBeAg may also be present in chronic.

For both conditions, HBsAg will be detected in blood, with no HBsAg for >6 months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is the mainstay of treatment for SBP? How long?

A

3rd generation cephalosporins, i.e. ceftriaxone
Short course: 5-7 days

Remember you are just trying to hit facultative anaerobes here, anaerobic infection is unlikely

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

How do we treat community acquired vs nosocomial or critically ill CA intra-abdominal infections? How long?

A

CA: treat E. coli empirically based on location with a cephalosporin + metronidazole for B fragilis

Nosocomial/Critically ill: Expand coverage to cover Pseudomonas, i.e. Cefepime /metronidazole or Piperacillin/tazobactam

Treat 4-7 days, or until WBC drops, fever drops, and GI function returns

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is critical for stopping intra-abdominal infections?

A

Source control - need to drain abscesses / check for resolution via MRI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Most common causes of daycare associated gastroenteritis?

A
  1. Rotavirus
  2. Shigella
  3. Giardia
  4. Cryptosporidium
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What diarrheal diseases do we always treat with antibiotics?

A
  1. Shigella
  2. ETEC
  3. Campylobacter
  4. C. difficile
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What diarrheal diseases do we avoid anti-motility treatment in?

A

Blood diarrhea, EHEC, C. difficile

-> all toxin-mediated (need to poop the toxins out)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Do we treat Salmonella with antibiotics?

A

Not routinely, unless severe disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What are the two recommended treatments for Salmonella / Shigella? How long in normal vs immunocompromised / relapsing patients?

A

Either Ciprofloxacin or Amoxicillin / Ampicillin (HELPS)

Salmonella normal: 5-7 days
Relapsing / compromised: 14 days

Generally, takes a few less days to treat Shigella

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

How long is E. coli treated?

A

3 days of Cipro or cephalosporins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What is the treatment for Aeromonas?

A

3 days of Cipro

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What is the number 1 treatment for Vibrio, and what do you do if you can’t use that agent?

A

Doxycycline 300 mg x 1 (triple the normal dose)

If child under 8, use TMP/SMX x3 days, or 1 dose FQ

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Why do we avoid fluoroquinolones in children for treatment of E. coli and what do we give instead?

A

Cartilage damage -> give Bactrim or cephalosporins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What is the duration of therapy for C. difficile?

A

10-14 days on first instance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What are the side effects of IFN-alpha?

A

Flu-like symptoms on administration

Long-term: Bone marrow suppression, severe depression of mood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What is the primary adhesion virulence factor of N. gonorrhoeae and how does it attach and evade host immune response?

A

Pili - binds human CD46 membrane receptor

  1. RNA level = Slipped strand mispairing - Change the pilus length and create pilus plus and pilus minus (do not survive) phenotypes
  2. DNA level = Antigenic variation, PilE = expression, must recombine with pilS (several loci) to express different amino acid sequence in pilus protein
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What causes the majority of damage in gonorrhea?

A

Immune response to lipo-oligosaccharide (Neisserial LPS which gets sialyted to evade neutrophil attachment)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

How can gonorrhea be detected in men vs women in the lab?

A

Symptomatic men = gram stains. Does not work for symptomatic women (need PCR).

Typically, just culture urethral discharge (men) or cervical swabs (women) on Thayer-Martin

Diplococci within PMN = diagnostic for men

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What is tertiary syphilis marked by?

A

Gummas - Granulomatous lesions of skin, bone, and joints due to host immune response. (noninfectious)

Neurosyphilis - Argyll-Robertson pupils (constricts on accommodation but does not react to light), tabes dorsalis, dementia, optic atrophy, seizures

Cardiovascular syphilis - Aortic aneurysm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

For severe cases of congenital syphilis, what are some of the pathopneumonic exam findings?

A
  1. Hutchinson’s teeth - notched teeth
  2. Saddle nose - bend in nose
  3. Hard palate defect
  4. Short maxilla
  5. Protruding mandible
  6. Rhagades - linear scars on edge of mouth
  7. CN8 deafness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What is the function of gp120?

A

Part of viral envelope, binds to CD4 and CCR5 or CXCR4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What are the four HIV accessory proteins?

A 
Nef = immune EEEEvasion by downregulating cd4 and mhc class 1
Vif = Viron infectivity factor - Counteracts cytIIIdine deaminases that degrade viral mRNA
Vpu = Virus bUUUUdding
Vpr = translational aRRRest
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What are Tat and Rev?

A

Tat = transcriptional activator -> upregulate viral mRNA synthesis

Rev = facilitates exit of viral mRNA from nucleus without splicing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What drug might be better than oral vancomycin for the treatment of C. difficile diarrhea?

A

Fidaxomicin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What is common in early onset neurosyphilis?

A

Meningitis

Tabes dorsalis + argyll-robertson pupil is more common in late onset

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What two labs are typically elevated in vaginal trichomoniasis?

A

Vaginal pH and PMNs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What STDs will increase transmission of HIV?

A

Inflammatory - will result in increase of CD4+ cells near the genitals - transmission is actually more likely to occur to higher CD4 counts

Ulcerative - leads to exposed mucus membranes (i.e. HPV, HSV, Syphilis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What three things can make you an elite controller?

A
  1. APOBEC3 - protein which interferes with reverse transcriptase
  2. CCR5 mutant
  3. CCR5-ligand is upregulated and competitive
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What is the longterm risk of elite controllers?

A

Chronic immune activation can produce premature vascular disease (atherosclerosis) as well as non-AIDS cancers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Other than a loss of cell-mediated immunity, what are two other degradations of the immune system which can occur in HIV?

A
  1. Disordered antibody production and overproduction of non-specific antibodies (heterophile antibodies like EBV)
  2. Bone marrow failure in late AIDS leading to severe NEUTROPENIA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What are the three main types of Pili on UPEC and what is their mannose-sensitivity (unable to work when a plate it covered in it)

A
  1. P-pili - mannose insensitive - binds globobiose via PapG
  2. Type 1 Pili - mannose sensitive (binds mannose via FimH)
  3. Type S fimbriae - mannose insensitive - bind sialic acid
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What two toxins are made by UPEC and what is their function?

A
  1. Hemolysin - causes kidney damage in pyelonephritis, used for iron acquisition
  2. Cnf1 - Cytotoxic necrotizing factor 1 -> kills human bladder epithelium by apoptosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What is a struvite stone?

A

Kidney stone - magnesium ammonium phosphate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

How is S. saprophyticus identified in the lab?

A

Grows on CNA agar (Gram positive), is catalase + (it’s Staph), catalase negative (not aureus), and novobiocin-resistant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What pili does K. pneumoniae have?

A

Type 1 - same as E. coli
Type 3 - mannose insensitive

Told apart from E. coli by being non-hemolytic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

How is Proteus mirabilis told apart from E. coli / Klebsiella?

A

It is lac negative

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Two major virulence factors of proteus?

A
  1. MR/P - mannose-resistant, proteus-like for pyelonephritis

2. Swarming motility to make it up ureter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What is PMF?

A

Proteus mirabilis fimbrae - like E. coli Type 1 Fimbriae but is not a hemagglutinin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

What is Asa1? Give 2 other Enterococcus virulence factors

A

Aggregation substance, a virulence factor of Enterococcus which fascilitates conjugal plasmid exchange for antibiotic resistance, and is also involved in adherence via integrins

  1. Cytolysin - for freeing up iron
  2. Sex pheromones - for mating and exchanging drug resistance factors, also attracting neutrophils
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

What is the purpose of fimbrial adhesins for E. coli?

A

Internalization via Dr blood group antigens to epithelial cells to evade immune response.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

What is recurrence vs relapse vs reinfection in UTI’s?

A

Recurrence = another UTI (about 25% will have another UTI within 1 year)

Relapse = recurrence with same micro-organism (usually <2 weeks)

Reinfection = recurrence with different micro-organism
(usually >2 weeks)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

What are the cases in which asymptomatic bacteriuria is treated?

A
  1. Pregnancy (bad outcomes for child)
  2. Prior to invasive instrumentation of urinary tract for a procedure (need to do a pre-culture)
    Questioned by Pogue:
  3. Renal transplant patient (during first 6 months post transplant)
  4. Neonates
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

What makes the junctions of the blood brain barrier vs blood-CSF barrier?

A

BBB - tightly joined endothelial cells surrounded by glial processes (i.e. astrocytes)
BCSFB - endothelial cells with fenestrations and tightly joined choroid plexus epithelium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What are the risk factors for meningitis caused by S. pneumoniae?

A

immunosuppression (i.e. HIV or recent influenza), distant foci of infection (i.e. chronic otitis media), or low levels of circulating antibodies to capsule

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

What produces a ring-enhancing lesion on CT?

A

Fibrotic capsule of polymicrobial abscesses, most often caused by Streptococcus species or anaerobes

Also Toxoplasma or Cryptococccus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

What are P1-P3 and what is their general function in picornaviruses??

A

CPR - all encoded by a single mRNA which has polypeptides cleaved

P1: C: Capsid proteins
P2: P: Processing proteins - includes 2A and 3C
P3: R: Replication of genome

73
Q

What receptor does polio use?

A

Pvr = polio virus receptor

74
Q

What are 3D and VPg?

A

Picornavirus proteins which must work together

3D = RNA-dependent RNA polymerase
VPg = viral protein G, binds the 5' UTR, provides polyU primer for RNA synthesis

IRES = Internal Ribosome Entry Site - binds ribosome in 5’ UTR, not present in Flavivirus except Hepacivirus

75
Q

What are the three major structural proteins for Flavivirus replication?

A
  1. C - capsid
  2. E - envelope
  3. PrM - protease for maturation
76
Q

What is antibody-dependent enhancement?

A

Antibody-dependent enhancement (especially dengue-virus)

Since flaviviruses mutate so quickly, previously protective antibodies bind but do not neutralize the new virions. These antibodies facilitate opsonization which allow viruses to more efficiently enter macrophages + enhance replication

77
Q

What is the most important flavivirus non-structural protein?

A

NS1 - soluble hemagglutinin which could become a vaccine target

78
Q

What is the thing to remember about Chikungunya virus?

A

“Bent out of shape” - arthritis and join symptoms - transmitted by Mosquito

79
Q

What to remember about EEE?

A

Small hemorrhages in brain + neuronal damage, very rare, otherwise similar to West Nile Virus

80
Q

Other than flu-like symptoms, what are the common early symptoms of Rabies?

Late?

A

Increased muscle tone and hydrophobia

Late: Confusion, agitation, cerebral dysfunction, hallucinations, hypersalivation, insomnia

81
Q

What is seen histologically in Rabies?

A

Cytoplasmic eosinophilic inclusions called Negri bodies (iNtEGRIty)

82
Q

What is the primary virulence factor of Viridans Streptococci?

A

Glucans (dextrans in sketchy) which permit attachment to teeth, caries.

S. mutans is associated with dental caries

83
Q

What three diseases do oral anerobes cause?

A
  1. Chronic marginal gingivitis
  2. Peridontitis - progression, between supporting tissue and teeth
  3. Acute necrotizing ulcerative gingivitis - trench mouth

can also form abscesses

84
Q

What allows Actinomyces to colonize and what is the progression of the infection?

A

Some trauma, often a dental operation, that penetrates the epithelial barrier. It is slowly progressing, leading to pus and bacteria which flow in sinus tracts which drain the pus directly onto the skin

In severe infection, aspiration may lead to thoracic actinomycosis

85
Q

What are the the physiological effects of increased cAMP in Pertussis? What is the severity of disease?

A
  1. Increased histamine sensitization
  2. Promotion of lymphocytosis in bloodstream by disabling lymphokine receptors which bring them out of the bloodstream. (sketchy Gi with overflowing popcorn)
  3. Insulin secretion
  4. Diminished oxidative killing via macrophages

This is also caused by invasive adenylate cyclase which increases PMN count and reduces killing

Fulminant disease in infants and young children (edema + brain hemorrhages), both adults / infants clear in 100 days

86
Q

What is the pathogenesis of pertussis?

A

Filamentous hemagglutinin lets Bordetella adhere to bronchiolar epithelium. Toxins kill the cilia and interfere with phagocytosis. Systemic effects are felt due to circulating toxin (increased cAMP). Local inflammation to bacterial in bronchi leads to cough.

87
Q

What is the morphology of pertussis?

A

Same as H. influenza -> gram negative coccobacillus

88
Q

What are the systemic manifestations of diphtheria?

A

Can cause myocarditis, arrythmias, and attack the CNS

89
Q

Is smallpox a centrifugal rash? Varicella?

A

Both are considered centrifugal

Smallpox - starts on face and spreads from proximal extremities and trunk to distal extremities, also considered centrifugal. There are more extremity lesions in smallpox

Varicella - starts on trunk and spreads outward, like the centrifugal force. There are more trunk lesions in varicella

90
Q

What are the two diseases caused by Legionella? What are the clinical characteristics?

A
  1. Legionnaire’s Disease - severe lobar pnuemonia causing hyponatremia, diarrhea, headaches, confusion, and high fever
  2. Pontiac fever - Shorter incubation, self limiting, malaise which is less severe than the pneumonia (less virulent or dead strains)
91
Q

What are the mechanisms by which Legionella enters the macrophage?

A
  1. Has surface protein for C3 binding and complement-mediated phagocytosis
  2. “Coiling phagocytosis” - induces alveolar macrophage uptake in the absence of opsonization via phagocytosis
92
Q

What is significant about Acetinobacter and what is its morphology?

A

It is multiple-drug resistant and nosocomial, with a high incidence in U.S. Gulf War soldiers. Causes pneumonia and blood/wound infections in immunocompromised

Morphology: gram negative coccobacillus (similar to H. influenzae or B. pertussis)

93
Q

What do Legionella, TB, Histoplasma, and Chlamydia all have in common?

A

They grow intracellularly inside macrophages

94
Q

What can predispose people to pneumonia via Aspergillus?

A

Asthma, chronic bronchitis, tuberculosis. immunosuppression

-> neutrophils are the primary defense

95
Q

What T / B cell combinations indicate a poor vs good response to Coccidioides?

A

Immunity is primarily T-cell mediated
Good: Strong T cell response with little antibody
Bad: Increased non-protective B cell response (complement fixation does not work)

96
Q

What is done to get a PCP sample?

A

Bronchoalveolar lavage for a sputum sample via hypertonic saline, especially in AIDS patients since they normally won’t produce sputum.

Can also biopsy

97
Q

What are the clinical symptoms of pneumocystosis? How do patients die?

A

Mild or low grade fever
Typical signs of pneumonia absent - NONPRODUCTIVE COUGH
Progressive dyspnea and tachypnea with cyanosis due to hypoxia.

Patients die by asphyxiation

Also is a trophozoite detected by Giemsa stain (although still a fungus)

98
Q

What is vasogenic edema?

A

Edema caused by increased permeability of blood brain barrier, leads to increased ICP, especially due to exit of proteins from the blood into the CSF leading to increased oncotic pressure

Basically, edema caused by “vaso” or vessels opening

99
Q

What is interstitial edema?

A

Increased resistance to CSF outflow due to inflammation of the subarachnoid space leads to increased ICP and breakage of blood-CSF barrier, but will NOT cause a protein increase

Basically, edema caused by excess CSF

100
Q

At what age do we again start worrying about Listeria and E. coli as meningitis causes again?

A

Age 50

101
Q

What is one really specific and important finding indicating meningitis in neonates / infants?

A

Bulging fontanelle

102
Q

What is most likely to cause meningitis post head trauma / surgery?

A

S. aureus and S. epidermitis, maybe some aerobes like E. coli and Pseudomonas

Only an issue in CSF leak / basilar skull fracture: H. influenzae and Group A Strept

103
Q

What is the most common cause of viral meningitis and who gets it?

A

Typically associated with enteroviruses (Polio and Cocksackievirus), most common in infants / young children in late summer and early fall

104
Q

What are important predisposing factors to meningitis?

A

OPS of MOPS, although direct seeding has not been shown,

Endocarditis, recent head trauma / CSF leak, immunosuppression or splenic dysfunction, alcoholism, complement deficiency

105
Q

What is one shared side effect of integrase inhibitors? One thing they all need to do in terms of a drug interaction necessity?

A

Binds divalent cations - give separately

All need to have doubled dose if given with rifampin

106
Q

What is the side effect of concern with colbicistat and raltegravir?

A

Both cause CPK elevations, colbicistat due to inhibition of excretion and raltegravir due to rhabdomylosis

107
Q

What is the cutoff GFR for giving tenofovir?

A

> 30 GFR is needed, because it’s nephrotoxic

108
Q

What is the only integrase given with a booster?

A

Elvitegravir -> only one which is CYP3A4 metabolized

109
Q

What is the best integrase inhibitor and a drug interaction we worry about?

A

Dolutegravir - once daily dosing

Doubles the effectiveness of metformin in diabetics -> hypoglycemic crisis

110
Q

What are the two most common 2-NRTI backbones?

A
  1. Abacavir / lamivudine

2. Tenofovir / emtricitabine

111
Q

What are the HIV major drugs which are CYP3A4 metabolized?

A

Ritonavir, Darunavir (All PIs)
Elvitegravir
Maraviroc

Pyramethamine for T. gondii is also CYP3A4
Pentamidine = CYP2C19

112
Q

What is the PCP treatment of choice?

A

High dose TMP/SMX for 21 days, with option of corticosteroids to reduce inflammation in moderate/severe

113
Q

What is the MAC treatment?

A

Two or more anti-mycobacterial drugs to prevent resistance.

First line: Clarithromycin + Ethambutol + sometimes rifabutin

114
Q

What is the prophylaxis for PCP and T. gondii? MAC

A

Both are TMP/SMX or dapsone

MAC is once weekly azithromycin or clarithromycin

115
Q

What is the treatment for PCP?

A

TMP / SMX x 21 days, +/- corticosteroids for moderate to severe inflammation

116
Q

What are the first line treatments for community-acquired pyelonephritis, given orally? Duration of therapy?

A

FQ (i.e. Cipro)
TMP/SMX
3rd generation Cephalosporin

Generally 7-14 days of therapy is fine, leaning towards 7

117
Q

What is the treatment for first episode of HSV-2?

A

Valacyclovir BID x7-10 days

118
Q

What organism should be considered for non-gonoccal urethritis if doxycycline was given?

A

Mycoplasma genitalium

A second, less likely cause of non-gonococcal urethritis.

Treat with moxifloxacin (assuming they had doxy due to azithromycin allergy)

119
Q

What are two uncomplicated gonococcal infections and what is the treatment?

A

Cervicitis, urethritis

Treatment: Ceftriaxone 250 mg IM x 1

+

Azithromycin 1g PO x 1 dose (always treat for chlamydia)

120
Q

What are the treatments for bacterial and fungal vaginosis? Trichomonas vaginalis?

A

Bacterial: Gardnerella - Metronidazole x 7 days
Fungal: Fluconazole x 1 dose

Trichomonas - Metronidazole x7 days, or just one dose of 2g metronidazole

121
Q

What is the treatment of epididymitis?

A

Ceftriaxone IM + doxycycline

Substitute levofloxacin for doxy if enteric organisms are a concern (cover pseudomonas)

122
Q

What is the empiric regimen for PID?

A

Cefoxitin to cover gonorrhea
+
Doxycycline to cover chlamydia

BOTH GIVEN IV until there is a response

123
Q

What are the drugs of choice for healthcare associated UTI?

A 
Cefepime or ceftazidime 
Zosyn 
Cipro / Levo 
Carbapenems minus ertapenem 
Aminoglycosides
124
Q

What does congenital varicella cause?

A

Mental retardation, cerebral atrophy, and non-CNS abnormalities (limb hypoplasia, blindness, cutaneous dermatomal scarring)

125
Q

What proportion of kids have clinical signs of CMV at birth if infected, and what are they?

A

10%: Intrauterine growth retardation, hepatosplenomegaly, microcephaly, blueberry muffin rash, ventriculomegaly

Majority will develop longterm sequelae including mental retardation, seizures, sensorineural hearing loss, and death

126
Q

What causes pathology in PML, a condition caused by JC virus?

Polyomavirus = circular dsDNA

A

PML - Progressive Multifocal Leukoencephalopathy
Demyelination of deep cortical white matter via replication in oligodendrocytes, with minimal inflammatory processes going on

127
Q

What does BK virus cause in immunocompetent vs immunocompromised hosts?

A

Immunocompetent: Mild upper respiratory disease (same as JC virus)

Immunocompromised:

  1. Polyomavirus nephropathy, especially in renal transplant patients.
  2. Hemorrhagic cystitis, in bone marrow transplant patients.
128
Q

Why do older people often get pneumonia?

A

Diminished ciliary clearance, abnormal elastic recoil of lungs, and diminished T and B cell response

129
Q

What is the morphology of Moraxella catarrhalis?

A

Gram negative diplococci, causes pneumonia in COPD patients

130
Q

What urine tests are run for pneumonia?

A
  1. Pneumococcal antigen

2. Legionella, serotype 1

131
Q

What microbes are frequently implicated in nosocomial pneumonias, and do we worry about Candida?

A

Gram negative aerobes (Pseudomonas, Acinetobacter)
MRSA

Candida is often cultured, but does NOT cause disease and should not be treated

132
Q

What are the X-ray features of aspergillosis? Risk factors?

A

Nodular lesions with “halo sign” that often progresses to cavities

Neutropenia, prolonged steroid use, and chronic granulomatous disease are risk factors

133
Q

What lab is usually elevated in PCP pneumonia?

A

Serum beta-glucan

134
Q

What are two lab signs that point to pneumonia?

A
  1. Elevated white cell count with left shift

2. High inflammatory markers (procalcitonin, C-reactive protein)

135
Q

What is one specific finding that happens in about 5% of Mycoplasma pneumoniae?

A

Bullous myringitis -> inflammation of the tympanic membrane

136
Q

What is a typical empiric treatment regimen for neutropenic patients?

A

Must cover P. aeruginosa

Piperacillin/tazobactam or cefepime or imipenem

PLUS

Aminoglycoside like tobramycin

137
Q

What diseases cause defects in Cell-mediated immunity?

A

Hodgkin’s lymphoma, non-Hodgkin’s lymphoma, Chronic Lymphatic Leukemia, hairy cell leukemia.

138
Q

What are four major immune defects associated with susceptibility to encapsulated organisms?

A
  1. Multiple myeloma
  2. Chronic lymphatic leukemia
  3. Waldenstrom’s macroglobulinemia
  4. Sickle cell disease
139
Q

What cancers and lymphomas is EBV associated with?

A

Burkitt’s lymphoma (Africans, bar kid, swelling cheeks), Nasopharyngeal carcinoma (asians), Hodgkin’s Lymphoma (Owl sitting in Reeds), Lymphomas / Lymphoproliferative tumors in AIDS

140
Q

What is Acute Respiratory Disease (ARD)?

A

Respiratory infection caused by Adenovirus commonly found in military recruits, transmission facilitate by stress and crowding.

Can cause mild URI to pneumonia

Only military has a vaccine

141
Q

What epidemic eye infection does Adenovirus cause and how is it spread?

A

Epidemic keratoconjunctivitis, spread by eyedroppers of healthcare workers

142
Q

What are two super uncommon adenovirus infections?

A

Urethritis and cystitis (think of statue of david peeing out blood into swimming pool transmission of pharyngoconjunctival fever)

143
Q

What are the symptoms of EBV infectious mono-nucleosis? How long does it last?

A

Common in adolescents and adults

Fatigue, fever, sore throat (pharyngitis, copious)

Specific: Lymphadenopathy (cervical, could be generalized), splenomegaly (due to T cell proliferation), lymphocytosis, and heterophile antibodies

Lasts 2-4 weeks acutely, with fatigue lasting longer

144
Q

What is the second phase of Parvovirus infection?

A

Deposition of immune complexes leads to erythematous rash + arthritis symptoms

145
Q

What is the first stage of Parvovirus B19 infection / where does it replicate / shed?

A

Nonspecific flu-like symptoms and suppression of reticulocytes (RBCs)

Replicates in bone marrow and sheds in Upper Respiratory Tract (probably URT transmission)

Parvoviruses are inactivated by protective IgM response

146
Q

What is the RNA complex called in Influenza, and what protein is involved in packaging nascent ones?

A

-sense RNA called Ribonucleoprotein (RNP)

M1 protein is a matrix protein involved in packaging new RNP’s and helping them bud out of the cell

147
Q

What is the function of the NS1 protein in Influenza?

A

blocks the interferon-induced RNaseL pathway

148
Q

What cleaves HA0 and what does it become?

A

Human protein trypsin, only present in lungs

Becomes HA1 - receptor for sialic acid and HA2 - transmembrane protein

149
Q

What is Measles Virus also called, and what are its prodomal symptoms?

A

Rubeola virus

Remember the 4 C's of the prodrome: 
Cough 
Coryza 
Conjunctivitis 
Coplik's spots
150
Q

What is the cell tropism of adenovirus?

A

Epithelial cells, including GI epithelium, URT, and conjunctiva of eyes (explains the wide range of illnesses it causes)

151
Q

What does Parvovirus replicate?

A

In the bone marrow, but starts in the upper respiratory tract

152
Q

What are the most common manifestations of mumps? Atypical?

A

Painful swelling of parotid glands (unilateral or bilateral), ear pain

Atypical:
Orchitis -> more severe, can cause infertility if bilateral
Also meningitis

153
Q

What do paramyxoviruses typically cause in adults?

A

Pneumonia and laryngitis (similar to croup)

154
Q

What is the empiric coverage we use for meningitis in patients <1 month?

A

Ampicillin + gentamicin or cefotaxime (3rd generation not ceftriaxone)

Gentamicin is okay because patient has no BBB

155
Q

What must be added onto the antibiotic regimen for adults >50 and why?

A

ampicillin, for listeria coverage

So regimen is:
ampicillin + vancomycin + ceftriaxone

156
Q

What is the empiric coverage for meningitis in patients 1-23 months of age and why?

A

Vancomycin + 3rd generation cephalosporin

Use vancomycin for possibility of mildly elevated MICs of Streptococcus pneumoniae which would not allow killing by cephalosporin in CSF

157
Q

Usually coag-negative staph (from skin)

Recommended broad therapy: Vancomycin + cefepime or ceftazidime

A

Usually coag-negative staph (from skin)

Recommended broad therapy: Vancomycin + cefepime or ceftazidime

158
Q

What is the most common causative pathogen in CSF shunt infections, and what is the recommended empiric treatment?

A

Usually coag-negative staph (from skin)

Recommended broad therapy: Vancomycin + cefepime or ceftazidime

159
Q

Who gets prophylaxis for meningitis caused by N. meningitis and H. influenzae and what is it?

A

N. meningitis - anyone exposed to oral secretions and household contacts - Ciprofloxacin 500 mg or rifampin

H. influenzae - everyone in a household with unvaccinated children (might spread to them) - Rifampin

160
Q

What is the first-line treatment for COPD exacerbation?

A

Doxycycline, with second-line amoxicillin/clavulanic acid, x3-7 days

161
Q

What is the therapy for sinusitis?

A

Same as outpatient COPD: amox/clav or Doxycycline

162
Q

What is given to healthy CA-pneumonia and high risk CA-pneumonia in outpatient therapy?

A

Previously healthy: azithromycin or doxycycline

High risk: beta-lactam + azithromycin or doxycycline

163
Q

For inpatient non-ICU CAP, what is the treatment?

A

Option 1: Azithromycin + 3rd gen cephalosporin
Option 2: Doxycycline + 3rd gen cephalosporin
Option 3: Respiratory fluoroquinolone

164
Q

What is the treatment of choice for outpatient aspiration pneumonia?

A

Amoxicillin/clavulanic acid (good gram negative / anaerobe coverage)

165
Q

What dictates the duration of therapy for community-acquired pneumonia?

A

Minimum of 5 days, must be afebrile for 48-72 hours, and no more than one “sign of instability”

  1. Fever, leukocytosis, tachycardia, tachypnea
166
Q

What is the empiric therapy for HAP/HCAP/VAP?

A 
1. Antipseudomonal beta-lactam 
\+ 
2. Antipseudomonal FQ or aminoglycoside 
\+ 
3. MRSA coverage: Vancomycin or linezolid

x7 days, assuming clinical response

167
Q

What are the drugs of choice for Stenotrophomonas as well as Listeria when patient is allergic to penicillin?

A

TMP/SMX

168
Q

What is the mechanism of Borrelia recurrentis antigen switching?

A

VMP - Variable major protein, a cell surface serotype

169
Q

What is the second stage of Lyme disease? Third stage?

A

Second: Bacteria spread to CNS and joints: Bilateral bell’s palsy and heart block (conduction defects). Possible early arthritis

Third: Encephalitis and polyarthritis likely, even in absence of organism

170
Q

Where does Rickettsia live?

A

Lives in vascular endothelium of lung, spleen, brain, and skin as an obligate intracellular organism (internalized via phospholipase)

171
Q

In what way is Bartonella infection of immunocompromised patients similar to Rickettsia?

A

Affects blood vessels.

While Rickettsia is the only one which is intracellular in the endothelium of lung, liver, brain, and skin,

Bartonella causes Bacillary angiomatosis which is a vascular infection as well. It can also cause hemorrhagic disease of spleen and liver

172
Q

Other than the Type 3 secretion system used to disrupt macrophages and PMNs, what other two virulence factors does Yersinia pestis have?

A
  1. Invasins - inducing actin rearrangement and uptake of bacteria into nonprofessional phagocytes
  2. Plasminogen activator - plasminogen will dissolve fibrin clots and prevent chemotaxis of PMNs
173
Q

What is the growth pattern of Francisella?

A

Intracellular, enters via skin lesion (i.e. tic bite), then travels to lymph nodes in macrophages before disseminating

174
Q

What does Bartonella usually cause?

A

Axillary lymphadenitis

175
Q

What is the incubation of smallpox vs chickenpox? Rash length?

A

Smallpox - 1-2 weeks
Chickenpox - 2-3 weeks

And smallpox lesions will last twice as long

176
Q

What are the four types of smallpox?

A

Common:

  1. Major
  2. Minor

Rare:

  1. Flat-type - flat, soft, focal skin lesions
  2. Hemorrhagic-type - mucosal hemorrhage and death before lesion formation
177
Q

What is the hallmark feature of ebola infections?

A

Massive hemorrhagic destruction of the liver. Also damage to spleen and kidney

178
Q

What illness does hantavirus cause?

A

Hantavirus pulmonary syndrome (HPS), along regular malaise symptoms including nausea or vomiting

HPS - respiratory distress syndrome which causes respiratory failure and pulmonary edema

Immuno mikro eng (56 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions