Brainscape's Knowledge GenomeTM

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


See full index

Immuno mikro eng > Upper Respiratory Tract Infections > Flashcards

Upper Respiratory Tract Infections Flashcards

1
Q

What is a primary vs secondary infection?

A

Primary - infectious organism is a pathogen
Secondary - infectious organism is an opportunist who strikes following a primary infection (i.e. viral pneumonia destroys innate immune system)

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

What is chronic marginal gingivitis?

A

Infection caused by oral anaerobes between teeth and gums, leading to inflammatory infiltrate in connective tissue associated with teeth.

Associated with improper tooth care - within 2 weeks

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

What is the primary virulence factor of oral anaerobes?

A

Release of PMN contents and complement activation exacerbates tissue damage - few virulence factors on their own

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

What is peridontitis?

A

The result of progressive gingitivits, leads to resporption of bone around neck of tooth, and loss of periodontal ligament and the tooth.

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

Where do the oral anaerobes typically live and what do they form?

A

Typically live in dental plaque and are polymicrobial autoinfections, causing abscesses

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

What is trench mouth?

A

Acute necrotizing ulcerative gingivitis, invasion of oral epithelium leading to bone resorption and tooth loss (similar to periodontitis)

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

What is the morphology and metabolism of Actinomyces israelii?

A

Gram positive, filamentous rods resembling fungi. It is an obligate anaerobe of the normal flora

Think Israeli soldier with purple bandage and branching tree in the background

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

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

How is Actinomyces identified?

A

Often by staining of pus, with “sulfur granules” being seen in the pus, diagnostic for infection.

Also, abscesses are usually polymicrobial as well, with gram negative rods.

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

What is the primary virulence factor of Viridans Streptococci? What is associated with dental caries?

A

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

S. mutans is associated with dental caries

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

How can Viridans cause endocarditis?

A

Can colonize damaged heart valves when you have transient bacteremia from tooth extraction

Think of the Jester wearing the damaged valve mitre

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

How is Viridans strept identified in the lab?

A

No Lancefield grouping, gram positive cocci which are catalase negative, optochin resistant

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

What is stomatitis? What is a common causative pathogen?

A

Inflammation of the oral cavity

Commonly oral thrush, caused by Candida albicans, on the tongue or palate. Appears and white cheesy plaques loosely adhering to mucosal surface

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

What are factors predisposing to oral candidiasis?

A
  1. Antimicrobial therapy depressing competing flora
  2. Immuncompromised - leukopenia, AIDS, corticosteroids
  3. Disruption of mucosa by indwelling devices
  4. Diabetes -> increases glucose concentrations and surface receptors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

In what way is Candida an AIDS-defining disease?

A

Esophageal candidiasis is very common in AIDS - loss of cell-mediated immunity (max 100 CD4 count / lbs in sketchy slide)

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

What are the predisposing factors to Streptococcal Acute Otitis Media?

A
  1. Viral infection
  2. Allergies
  3. Young age - eustachian tubes are shorter and more pliable than adults, so they drain worse
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How does otitis media occur?

A

Bacteria enter middle ear from naopharynx, and S. pneumonia has a high nasopharynx carrier rate (10-30%), predisposing people to URIs

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

What is another non-serious infection caused by S. pneumoniae?

A

Sinusitis, acute and chronic common of all age groups

Following allergies, viral infection, of anatomical obstruction

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

When is needle aspiration used?

A

Diagnosis of S. pneumoniae otitis media or sinusitis typically made clinically, however

Needle aspiration can be used to collect fluid behind tympanic membrane in cases of otitis media, or for sinus wall puncture in sinusitis

20
Q

What infection does H. influenzae typically cause, and in what age group?

A

Sinusitis and otitis media, especially in children less than 5 years old

21
Q

What are the common types of H. influenzae in the Upper Respiratory Tract and what is the carriage rate?

A

capsular serotypes a-f, we only vaccinate for hib but all can cause sinusitis / otitis, just hib leads to meningitis

Carriage rate is even higher than pneumococcus -> 50-80%

22
Q

What is the normal function of M protein of GAS?

A

Antigenic variability which is anti-phagocytic and anti-opsonic

23
Q

What two diseases are associated with GAS caused by antibodies cross-reactive with M protein?

A
  1. Acute glomerulonephritis

2. Rheumatic heart disease

24
Q

What does SLO due?

A

Streptolysin O -> causes Beta-hemolysis on blood agar plates, forming large pores in cell membranes.

25
Q

What is the mechanism of Spe A-C?

A

Similar to staphylococcal exotoxins, induces cytokine release via superantigenicity, which stimulates T cells and suppresses B cells.

26
Q

Why is prompt antimicrobial therapy required in Group A Strept pharyngitis? Is this the etiology of most pharyngitis?

A

Circumvents natural development of type-specific immunity to M protein, which causes post-streptococcal sequelae

Most pharyngitis is viral

27
Q

What are the features of Scarlet Fever and what causes it?

A

Caused by pyrogenic exotoxins (Spe)

Leads to scarlet rash which spreads from mouth and face to trunk and extremities; also “strawberry tongue”

28
Q

What are the features of Rheumatic heart disease and what does it follow?

A

Follows about 3 weeks after pharyngitis (not skin infection), preventable by treatment with penicillin

J: joints - polyarthritis
O = heart: carditis and other heart problems
N: Nodules - subcutaneous
E: Erythema marginatum - pink rings on torso or inner surface of limbs
S: Sydenham’s chorea - choreic movements of all four limbs

29
Q

What valve does rheumatic heart disease typically affect, and what is the mechanism?

A

Mitral valve

Mechanism is anti-M antibodies cross react with cardiac sarcolemma, smooth muscle cells, and valves

30
Q

What are the features of post-streptococcal sequelae acute glomerulonephritis and what does it follow?

A

Follows respiratory but typically skin infection via Group A strept

10-14 day latent period following infection, followed by edema often of the face, hypertension and lesion of glomeruli

Due to anti-M protein antibodies reacting with glomerular proteins, and Type 3 hypersensitivity

31
Q

How can Group A strept be detected in the lab?

A

Clear zone around colony on blood agar plate due to SLO, beta-hemolytic, catalase negative (not Staphylococcus), bacitracin sensitive (basset hound eating the pastry)

Morphology: Gram + cocci in chains

32
Q

What is the rapid strep test?

A

Nitrocellulose strip with antibodies to Group A Strept antigens

33
Q

What blood marker is seen in patients with rheumatic fever?

A

Anti-SLO (ASO) antibodies

34
Q

Why is Corynebacterium diphtheriae called a toxinosis?

A

Toxin is required for the disease - if you are colonized with diphtheria in the absence of diphtheria toxin, there is no pathogenesis. It is a true “virulence factor”

35
Q

What is the mechanism of diphtheria toxin?

A

AB toxin. A = activity, ADP-ribosylates EF-2 of any eukaryotic cell, which is required for ribosomal translocation, leads to stopping of translation

(same mechanism as pseudomonas exotoxin A).

36
Q

Where does C. diphtheriae typically colonize?

A

Human pharynx - causes diphtheria, very rare in the US due to Tdap. It is spread by aerosol transmission of droplets?

37
Q

What is seen in the oropharynx due to diphtheria?

A

Pseudomembrane (similar to C. difficile) which is not easy to move. Due to cytotoxicity.

38
Q

What is the morphology of C. diphtheriae?

A

Gram positive, club-shaped rods

39
Q

What are the systemic manifestations of diphtheria?

A

Can cause myocarditis and attack the CNS

40
Q

What is the pili for pertussis and what is its function?

A

Filamentous hemagglutinin - helps it adhere to ciliated (bronchiolar) mucosal epithielial cells. Also agglutinates RBCs and directs B. pertussis to macrophages

41
Q

What is the major toxin of pertussis?

A

Pertusiss toxin - an AB 1:5 toxin, which ADP-ribosylates the Gi protein (think of the injured GI in the sketchy), leading to an increase in cellular AMP levels

42
Q

What are the the physiological effects of increase cAMP?

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
43
Q

What is the other big toxin pertussis has? What is the net effect?

A

Invasive adenylate cyclase, which directly stimulates cAMP production via binding calmodulin.

Net effect: Interference with chemotaxis and superoxide production by PMNs (lymphocytosis + killing is diminished)

44
Q

Who is pertussis typically seen in, and what is the presentation in each group?

A

Typically seen in infants and preschoolers

Both groups show a prolonged (100 days) disease with paroxysmal coughing fits (sudden onset), leading to gasping of air (whooping)

Infants: bad cough, can cause edema and hemorrhages in brain
Adults: persistent cough, often undiagnosed

45
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.

46
Q

How is Bordetella grown in the lab? How is diagnosis made?

A

Deep nasopharyngeal cultures collected from patient, and cultured immediately

Grown on Bordet-Gengou or Charcoal blood agar + antibiotics media for isolation. Growth is very slow

Diagnosis is typically made via direct fluorescence antibody, but confirmed via culture

47
Q

What is the morphology of B. pertussis?

A

Gram negative coccobacillus.

Immuno mikro eng (56 decks)

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