Brainscape's Knowledge GenomeTM

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


See full index

Microbiology > Airborne Diseases > Flashcards

Airborne Diseases Flashcards

You may prefer our related Brainscape-certified flashcards:
Biology 101 flashcards
1
Q

Streptococcus pyogenes (Virulence Factors)

A

M Protein
Exotoxins
Streptolysin S & O

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

Exotoxins (Streptococcus pyogenes)

A
  • responsible for fever and symptoms of Toxic Shock Syndrome and Scarlet Fever
  • certain strains carry a lysogenic bacteriophage that encodes streptococcal pyrogenic exotoxins
  • these exotoxins act as superantigens
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

M Protein (Streptococcus pyogenes)

A

cross reactive antibodies cause Rheumatic Fever

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

Streptolysin S & O (Streptococcus pyogenes)

A

Cytolytic enzyme: lyse white blood cells, red blood cells, and platelets

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

Streptokinase (Streptococcus pyogenes)

A

Cytolytic enzyme: lyse blood clots to facilitate spread of S. pyogenes in tissues

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

Symptoms: Rheumatic Fever

A

Symptoms: inflammation of heart, joints, blood vessels, & subcutaneous tissues causing irregular heart rhythms & joint pain

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

Rheumatic Fever: Secondary disease to what bacteria?

A

Streptococcus pyogenes

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

Causes: Rheumatic Fever

A

Cause: S.pyogenes strains with cell surfaces antigens (M Protein) similar to heart valve and joint proteins

Antibodies directed at streptococcal antigens cross-react with the patients heart valve & joint proteins
Similar to autoimmune disease

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

Capsule (Streptococcus pyogenes Virulence factor)

A

Anti-phagocytic
Allows survival on surfaces
Made of hyaluronic acid

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

Virulence Factor: Rheumatic Fever

A

M Protein

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

Streptococcus pneumoniae diagnosis

A
  • Culture of Bacteria

- detection of G+ diplococci in sputnum

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

Streptococcus pneumoniae - Role of capsule in virulence/pathogenesis

A

Capsule

  • Determines different strains
  • Increases invasiveness
  • Prevents mucus entrapment
  • Prevents certain types of phagocytosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Bordetella pertussis: What stage is one most contagious?

A

Stage 1 - Catarrhal Stage - may last 1-2 weeks. low grade fever, mild, occasional cough

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

Bordetella pertussis: What is happening during coughing fits?

A
  • a massive build up of mucus & white blood cells in the lungs.
  • This blocks the airways preventing the patient from breathing.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Bordetella pertussis: In what age group is disease most severe?

A

Infants less than a year

  • Lack of immunity
  • Severe disease; almost always requires hospitalization
  • Can be fatal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Bordetella pertussis: Why is the pertussis vaccine recommended for pregnant mothers in every pregnancy?

A
  • Pregnant women: every pregnancy in third trimester
  • Maternal antibodies are passed to fetus
  • Antibodies are protective for roughly first 2 months of life
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Bordetella pertussis: Pathogenesis

A

Fimbriae - allow attachment to ciliated respiratory epithelial cells

Toxins - allow the bacteria to hide from the immune system & cause damage to lung tissue.

Damage to Lung Tissue - present on lungs of recovered patients several weeks after the cough & bacteria have been cleared making the patient susceptible to secondary bacterial or viral infections

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

Mycobacterium tuberculosis: What is mycolic acid

A

what the cell wall is made up of. The M. tuberculosis is very lipid rich made up of mycolic acid.

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

Mycobacterium tuberculosis: Where is mycolic acid found

A

in the cell wall

20
Q

Mycobacterium tuberculosis: What does mycolic acid make M. tuberculosis resistant to?

A

disinfectants and lab gram staining so acid fast stain is used instead. It is acid fast positive

21
Q

In what type of cell does M. tuberculosis replicate?

A

macrophages

22
Q

Mycobacterium tuberculosis: What are granulomas and how are they formed?

A

2) Inside macrophage bacteria inhibit phagocytic killing by: preventing phagolysosome formation or resisting killing by toxic oxygen
3) Bacteria attract more macrophages to area of infection that fuse to form multinucleated giant cells
4) In addition, the host attempts to “fight” infection by sending more macrophages & immune cells to the site of infection.

23
Q

granuloma

A

granuloma = compact & organized aggregate of immune cells attempting to limit spread of infection

24
Q

What is latent/dormant TB?

A

Ganulomas can become encased in scar tissue & become necrotic & caseous preventing immune cells from killing all of the bacteria, so viable bacteria can remain in the granuloma for months to years

25
Q

Who will test positive with a TB skin test?

A

Active TB, asymptomatic TB, latent TB & individuals who’ve received the BCG vaccine ALL test POSITIVE
Can NOT determine stage of infection

Identifies response to pathogen-specific inflammatory Th1 cells = delayed type hypersensitivity (test read @ 48hrs)

26
Q

Is treatment of TB short-term or long-term? Why?

A

Intensive phase:
isoniazid, rifampin, ethambutol, & pyrazinamide
daily for up to 2 months
Continuation phase:
Isoniazid & rifampin
2 to 5 times a week for 4.5 months
Purpose: to prevent reactivation of latent TB

27
Q

What is the definition of meningitis?

A

Inflammation of the meninges, the membranes that are the protective covering of the central nervous system (brain & spinal cord)

Attaches to cells of nasopharynx & gains access to the bloodstream causing widespread bacteremia and upper respiratory tract symptoms

28
Q

Meningitis: Symptoms

A

Sudden onset of headache, fever, & stiff neck
can progress to comma & death
Nausea, vomiting, photophobia, confusion
Meningococcemia (occurs in 10% of cases) – N. meningitides bacteremia,

29
Q

Meningitis: Diagnosis

A

Gram-negative diplococci in cerebral spina fluid is diagnostic

30
Q

Meningitis: Who is at risk?

A

Often occurs in epidemics in populations living in close proximity
Military barracks
College dorms

Incidence is much higher in:
Infants
School-aged children
Young adults
Sub-Saharan Africa: meningitis belt
31
Q

Meningitis: Role of Opa proteins and capsule in virulence and infection

A

Outer membrane proteins

  • Antigenic variation - change sequence & structure to hide from immune system
  • Adhesion and invasion of host cells

Capsule
Prevents phagocytosis

32
Q

What family of viruses causes almost all colds?

A

Rhinovirus

33
Q

Symptoms: cold vs flu

A

Rhinitis – inflammation of the nasal region
Nasal obstruction
Water nasal discharge
Muscle aches
General feeling of malaise, usually without fever

34
Q

How is each strain in the Influenza Virus identified?

A

Each strain is identified by a unique set of surface glycoproteins
- Hemagglutinin (H)
- Neuraminidase (N)
Each virus has one type of hemagglutinin and one type of neuraminidase on its virus capsid
The virus is named for the antigens it contains
Example: H1N1

35
Q

Hemagglutinin (HA)

A

HA; H antigen

Attachment to host cells

36
Q

Neuraminidase (NA)

A

NA; N antigen

Release from host cells

37
Q

Purpose of HA and NA?

A

Antibodies can recognize & bind HA or NA; stopping infection

38
Q

Antigenic drift

A
  • Minor changes in influenza virus antigens due to gene mutation
  • Result: host immunity to a given virus strain diminishes & reinfection with the mutated strain can occur
  • Reason last year’s flu vaccine does not work the next year
39
Q

Reassortment (Influenza)

A
  • Mixing of gene segments between different strains of influenza
  • Occurs when more than one strain infect the same host
  • reassortment of human and bird virus inside a pig forms a highly virulent reassortment virus
40
Q

Antigenic Shift

A

brought on by Reassortment

  • Major change in a surface antigen
  • Results from total replacement of the RNA that encoded that particular surface antigen
  • responsible for pandemics
41
Q

Koplik’s Spots

A

Measles

  • White dots inside mouth that are an early sign of infection
  • Rash occurs 3-5 days after spots
  • Easiest way to diagnose the infection
42
Q

Symptoms of Measles

A 
high fever,
cough,
runny nose (coryza), and
red, watery eyes (conjunctivitis).
Red rash shows up 2-5 days after infection
43
Q

Parotitis (mumps)

A
  • Parotid gland inflammation. This inflammation can lead to parotitis
  • The only know virus to cause parotitis epidemic
  • Virus replicates in these glands
44
Q

Congenital Rubella Syndrome (CRS)

A 
condition that occurs in developing babies of an infected mother. can cause:
Deafness
Cataracts
Heart defects
Intellectual disabilities
Liver and spleen damage
Low birth weight
Skin rash at birth

NO CURE!

45
Q

Lytic form of Varicella Zoster virus causes what disease?

A

Chicken Pox

46
Q

What type of cell does the Varicella Zoster virus go latent in?

A

human ganglia

47
Q

What disease does the reactivation of Varicella Zoster virus create?

A

Shingles

Microbiology (7 decks)

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