Brainscape's Knowledge GenomeTM

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


See full index

Infectious Disease > Week 5 > Flashcards

Week 5 Flashcards

1
Q

“Great neglected disease of mankind”

A

pneumonia often misdiagnosed, mistreated and underestimated

high cause of mortality

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

Pneumonia

infection of what?
typical presenting signs/symptoms?

A

infection of pulmonary parenchyma from the alveoli (LOWER respiratory tract infection)

Acute, fever, tachypnea, cough, purulent sputum, lung consolidation

Pleuritic chest pain

Infiltrate on CXR

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

Community Acquired Pneumonia (CAP):

Typical: SYMPTOMS

A

purulent sputum, gram stain may show organisms, typically LOBAR infiltrate on CXR

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

Lobar pneumonia

what is it?
3 bugs that cause this?

A

intra-alveolar exudate and consolidation

S. pneumoniae (#1), Legionella, Klebsiella

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

Bronchopneumonia

what is it?
4 bugs that cause this?

A

acute inflammatory infiltrates from bronchioles into adjacent alveoli

Patchy distribution can be >1 lobe

S. pneumoniae, S. aureus, H. influenzae, Klebsiella

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

5 bugs that can cause typical CAP

A

1) Strep. Pneumoniae = #1 cause of CAP, can be secondary pneumonia after viral infection
2) H. Influenzae = often secondary pneumonia s/p virus + COPD
3) Moraxella catarrhalis
4) S. aureus = abscess, empyema, #2 most common CAP
5) Klebsiella = aspiration of enteric flora, currant jelly sputum, abscess

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

Community Acquired Pneumonia (CAP):

Atypical: SYMPTOMS

A

cough prominent +/- purulent sputum, gram stain with PMNs, but few organisms, PATCHY or DIFFUSE infiltrate on CXR

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

Atypical CAP Bugs

A

1) Mycoplasma pneumoniae
2) Chlamydophila pneumoniae
3) Legionella pneumophila = CAP, pneumonia + COPD/immunocompromised
4) Influenza, RSV, adenovirus

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

Interstitial pneumonia

A

diffuse patchy inflammation localized to interstitial areas at alveolar walls

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

Pneumonia caused by viruses like Influenza, RSV, and adenovirus can be complicated by ________, _________ and ______ secondary bacterial pneumonias

A

can be complicated by S. pneumoniae, S. aureus, and Group A strep

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

Fungal causes of pnuemonia (4)

A

Histoplasmosis, Blastomycosis, Coccidiomycosis, Aspergillus

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

Treatment of pneumonia:

1) Previously healthy outpatients → ?
2) Outpatients with comorbidities → ?
3) Inpatients (not ICU) → ?
4) ICU patients → ?

A

Previously healthy outpatients → Macrolide, Doxy

Outpatients with comorbidities → Respiratory Fluoroquinolone (levo or moxi), Macrolide + Amoxicillin/Clav

Inpatients (not ICU) → Respiratory Fluoroquinolone, Macrolide + B-lactam (3rd gen cephalosporin)

ICU patients → 3rd gen cephalosporin + respiratory fluoroquinolone or macrolide

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

Pneumococcal vaccine:

23-valent pneumococcal vaccine

A

for ADULTS: effective for bacteremia (systemic infection), not effective for pneumonia (mucosal infection)

Given to adults > 65 and asplenic patients

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

Pneumococcal vaccine:

13-valent pneumococcal conjugate vaccine

A

given to CHILDREN<5 and adults > 65 = polysaccharide capsule + protein conjugate

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

Haemophilus Influenzae:

gram?
size?
shape?
Requires what for growth?
capsule?
A

Small, gram-negative bacillus (coccobacillus)

Requires NAD (factor V), and heme (factor X) to grow on CHOCOLATE AGAR

can be encapsulated or unencapsulated

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

encapsulated (typeable) H. influenzae

A

positive quellung reaction (ab bind to bacterial capsule and can be visualized under microscope)

6 encapsulated serotypes (a-f)

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

Which serotype is the most virulent H. influenzae?

which is the most predominant?

A

Serotype b = most virulent

Serotype a is most predominant type

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

Unencapsulated (nontypeable) H. influenza causes what kinds of diseases?

A

upper respiratory tract infections (noninvasive sinusitis, otitis media)

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

Haemophilus Influenzae:

Virulence factors: (3)

A

1) Polysaccharide capsule → necessary for bug to produce invasive disease
2) Endotoxin (LPS)
3) IgA protease

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

Haemophilus Influenzae:

IgA protease allows this bug to do what?

A

colonizes upper respiratory tract, and can spread via lymphatics to seed meninges = meningitis

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

Haemophilus Influenzae:

Transmission

-who is particularly susceptible to infection?

A

aerosol droplets

Often occurs in immunosuppressed, ASPLENIC patients, and children (after maternal ab protection has declined)

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

Haemophilus Influenzae:

Treatment?

A

40% resistance to ampicillin (can use for mucosal infections)

Use 3rd gen cephalosporins for meningitis

Chloramphenicol (highly toxic though)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Haemophilus Influenzae:

Diseases (7)

A

1) Septic Arthritis
2) Epiglottitis → “thumbprint” sign on XR
3) Meningitis
4) Otitis media
5) Pneumonia
6) Conjunctivitis
7) Sinusitis

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

Haemophilus Influenzae:

Vaccine? what strain does it work against? who gets it and when?

A

Hib vaccine: capsular polysaccharide (polyribosylribitol phosphate, PRP) of type B strain conjugated to diphtheria toxoid

Given from 2-18 months of age

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

Neisseria Meningitidis

gram?
shape?
ferments what?

A

Gram-negative diplococcus, “coffee bean” shape

Ferments glucose and maltose (gonorrhea only ferments glucose)

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

Neisseria Meningitidis

vaccine? against what strains? Given to who?

A

Vaccine against serogroups A and C (but NOT for serogroup B strains)

quadrivalent meningococcal conjugate vaccine (excluding Type B strain)

Given to high risk individuals 2-55 - teenagers previously unvaccinated

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

Neisseria Meningitidis

Virulence factors:

A

1) Polysaccharide capsule
2) IgA protease → cleaves human IgA
3) Lipooligosaccharide

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

Neisseria Meningitidis

Lipooligosaccharide allows bug to do what?

A

induce sepsis, facilitates immune evasion

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

Neisseria Meningitidis

Polysaccharide capsule allows bug to do what? who is susceptible?

A

necessary for bug to produce invasive disease

ASPLENIC patients at increased risk for septicemia

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

Neisseria Meningitidis

serotypes?

A

9 different serotypes

A, B, and C → responsible for most disease

B = N-acetyl neuraminic acid - NON immunogenic in humans because this is in humans too
→ NO group B vaccine

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

Neisseria Meningitidis

Diseases (2)

A

1) Meningitis

2) Meningococcemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Neisseria Meningitidis

Meningitis

  • symptoms (characteristic sign?)
  • who gets it?
  • major complications?
A

most common cause of bacterial meningitis from 6mo-6yrs and young adults (high school, and college age - living in close quarters)

SX: sudden onset fever, nausea, vomiting, headache, mental status change, myalgias, petechial rash**

Waterhouse-Friderichsen Syndrome: due to LOS endotoxin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Neisseria Meningitidis

Treatment/Prophylaxis

A
  • 3rd and 4th gen cephalosporins or penicillin G
  • Not a big problem with resistance

Prophylaxis: RIFAMPIN (given to close contacts), ciprofloxacin, or ceftriaxone

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

Neisseria Meningitidis

Transmission

A

Normally colonizes nasopharynx epithelium

Transmission via respiratory droplets

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

Streptococcus Pneumoniae (pneumococcus)

gram?
shape?
grows on what agar?
anaerobe/aerobe?
optochin?
hemolysis?
catalase?
quelling reaction + or -?
A

Gram-positive diplococcus, “lancet shaped”

Grows on blood agar

Facultative anaerobe

Optochin sensitive

Alpha-hemolytic

Catalase negative

Positive quellung reaction

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

Streptococcus Pneumoniae (pneumococcus)

Virulence factors (2)

A

1) Polysaccharide capsule → necessary for bug to produce invasive disease
2) IgA protease → colonizes respiratory tract

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

Streptococcus Pneumoniae (pneumococcus)

Serotypes?

A

90 different capsular serotypes - only 12 cause infection

Serotype H. influenza b capsule can cross react with S. pneumoniae → can get misdiagnosis of H. influenzae or S. pneumoniae

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

Streptococcus Pneumoniae (pneumococcus)

Diseases? (5)

A

1) Meningitis
2) Otitis media (in children)
3) Pneumonia (< 2 years, > 65 years) = rusty brown sputum
4) Sinusitis
5) Conjunctivitis

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

Streptococcus Pneumoniae (pneumococcus)

Meningitis

A

most common cause of bacterial meningitis in all adults

Increased risk for infection with: asthma, viral infection, smoking, asplenic, immunocompromised

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

Streptococcus Pneumoniae (pneumococcus)

Treatment

A

Alarming multidrug resistance increasing

Respiratory fluoroquinolone (levofloxacin, moxifloxacin)

B-lactam + macrolide/doxycycline

Vancomycin is only available antibiotic in some places

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

Mycobacteria

anaerobe or aerobe?
stable or labile?
grown on what agar?

A

Strict aerobes

Very stable (can remain virulent in dried sputum for 6-8 months)

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

Mycobacteria

Cell wall features? (4)

A

1) Outer lipids and proteins → used for PPD test
Very thick outer lipid layer

2) Lipoarabinomannan (LAM) layer
3) Phosphatidylinositol Mannoside (PIM) layer
4) Mycolic acids (long chain lipids)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Mycobacteria

Mycolic acids

-what stain uses this feature?

A

Mycolic acids (long chain lipids) → hardy, difficult to stain → ACID FAST

Ziehl-Neelsen Stain (carbol fuchsin)

Increases bacterium’s virulence

Targeted by INH

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

Mycobacteria Tuberculosis

A

acid-fast (red), obligate aerobic rod

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

Mycobacteria Tuberculosis

Virulence factors? (3)

A

Mycolic acids
Cord factor
Sulfatides

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

Mycobacteria Tuberculosis

Cord factor

A

inhibits macrophage maturation and induces TNF-a release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Mycobacteria Tuberculosis

Sulfatides

A

surface glycolipids that inhibit phagolysosomal fusion

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

Mycobacteria Tuberculosis

Transmission

A

airborne microscopic droplets, human-to-human spread

High risk settings: prisons, hospitals, homeless shelters

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Mycobacteria Tuberculosis

Initial infection, replication, and spread →

A

Initial infection, replication, and spread → TB reaches alveoli and is phagocytosed by alveolar macrophages → replicates in macrophages

Carried by macs and DCs to draining lymphatics → blood → other organs

PIM, ManLAM, and SapM components of TB cell wall prevents phagosome/lysosome fusion and promotes growth within macrophages

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

TB granuloma (tubercle) formation:

A

TB in center, contains components on cell wall that promote granuloma formation

Macrophages come in and kill TB → necrotic center and formation of giant cells (fused macrophages)

T cells produce INF-y and TNF-a

Calcification and fibrosis surrounding center

Bacteria confined in “tubercles” = granulomas with epithelioid cells, giant cells, and lymphocytes + necrotic center (caseous necrosis)

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

What type of immunity is responsible for fighting TB?

A

Cell-mediated immunity develops at 2-6 weeks dominated by TH1 cells

Infection controlled via CMI, humoral immunity does NOT play a major role, but is used as a diagnostic tool

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

Alveolar macrophages, monocytes, and dendritic cells: Role in TB

A

critical for processing and presenting antigens to T cells (CD4+ and CD8+) → activation and proliferation of CD4+ cells → differentiate to TH1 and TH2

Site of replication for TB

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

TH1 cells and TB

TH1 cells release ______

TH1 cells also release ______ –> activate ______ and ________ which then release ______

A

TH1 →

IL-2

IFN-y → activate macrophages and monocytes

Macrophages release cytokines (TNF-a)

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

TH2 cells release what cytokines in response to TB infection? (4)

A

TH2 → IL-4, IL-5, IL-10, IL-13

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Pulmonary TB

A

(most common)

Cough (> 3 weeks)

Night sweats, chills, fever, weight loss

Hemoptysis

  • Ghon focus
  • Ghon Complex
  • Ranke Complex
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Ghon focus

A

granuloma located near pleura in middle or lower lobes with central caseous necrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Ghon complex

A

ghon focus + regional (usually perihilar) lymphadenopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Ranke complex

A

Ghon complex that has undergone progressive fibrosis and subsequent calcification from cell-mediated immunity (radiologically detectable)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Extrapulmonary TB:

A

1) Scrofula
2) Pleural or pericardial effusion
3) Kidneys → malaise, dysuria, gross hematuria, sterile pyuria
4) Pott’s disease
5) Joints (chronic arthritis)
6) CNS

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

scrofula

A

Extrapulmonary TB disease

Cervical Lymphadenitis (scrofula) = painless, chronic neck mass

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

Pott’s disease

A

Extrapulmonary TB disease of the Spine → Pott’s disease (infection of spine, destruction of intervertebral discs and vertebral bodies)

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

Extrapulmonary TB disease in CNS

A

CNS → Meningitis, granulomas in brain BASE

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

Miliary TB

A

disseminated TB

More common in HIV patients

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

Outcome of TB exposure:

A

1) 30% of those exposed are infected → 5% have early progression to primary disease (typically immunocompromised), 95% develop latent infection (immunocompetent)
2) Those that have latent disease → 5% get secondary/reactivation TB (due to reduced immune function, TNF-a therapy), and 95% will continue to contain the TB in latent form

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

Active TB disease

A

active, multiplying tubercle bacilli in the body

Positive PPD test

CXR ABNORMAL

Sputum smears and cultures usually positive

SX = cough, fever weight loss

Infectious before treatment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Reactivation TB

A

secondary disease

Cavitary lesions in UPPER lobes

Very infectious

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

Latent TB

A

inactive, contained tubercle bacilli in the body

Positive PPD test

CXR usually normal

Sputum smears and cultures negative

No symptoms, not infectious

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

PPD Test

-what causes a false positive, what causes the false negatives?

A

Latent TB diagnosed via PPD+ skin test (once exposed to TB, will have PPD+ for life)

False positive PPD can occur with BCG vaccine AND NON-TB mycobacteria

False negative PPD with steroid use, malnutrition, immunocompromised states

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Quantiferon Gold assay

A

IFN-y release assay, measures IFN-y in serum released from T cells exposed to TB (does NOT cross react with PPD)

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

Treatment of TB

A

Active TB → RIPE therapy

Rifampin
Isoniazid
Pyrazinamide
Ethambutol (or streptomycin)

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

Prophylaxis for latent TB →?

A

Isoniazid (9 months) + Pyridoxine (B6)

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

BCG vaccination

A

live attenuated vaccine, induces cell-mediated immune response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

TB skin test results:

1) HIV infection, contact to active TB case, abnormal CXR, or immunosuppression –> ______ mm is considered a positive PPD
2) Recent imigrants, injection drug users, children, high risk medical conditions, residents/employees of jails/nursing homes, hospitals –> ______ mm is considered a positive PPD
3) No risk -> ______ mm is considered a positive PPD

A

1) > 5mm
2) > 10mm
3) > 15 mm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Nontuberculous Mycobacteria

Symptoms are due to what?
causes what kind of infection?
transmission?

A

Constitutional symptoms due to TNF-a (NOT bug itself)

Causes chronic infections, often drug-resistant

transmission between humans, acquired from environmental sources (soil, water) via inhalation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Mycobacterium avium complex (MAC)

disease?
affects who?
how does it get into the body?

A

Disease: nonspecific symptoms - cough (productive or dry), fatigue, malaise, weakness, dyspnea, chest discomfort, hemoptysis

Systemic disease, multi-organ involvement

HIV patients with CD4 < 50 at HIGH RISK

NOT contagious to general population

Initial portal of entry is often GI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

How can you differentiate TB vs. MAC

A

Distinguish from TB by presence of: anemia, high alk phos, high LDH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Diagnosis, treatment, prophylaxis of MAC

A
  • Diagnosis: Acid-fast bacilli within macrophages on histology
  • Treatment: azithromycin or clarithromycin/ethambutol
  • Prophylaxis: azithromycin or clarithromycin (used in HIV CD4 < 50)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Mycobacterium kansasii

A

pulmonary and systemic disease - very similar to TB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

Mycobacterium marinum

A

found in water sources

Causes papules or ulcers in lymphocutaneous pattern
Seen in aquarium cleaners, fishermen, seafood handlers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Mycobacterium abscessus

A

pulmonary + cutaneous disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

Mycobacterium ulcerans (Buruli ulcer)

A

skin disease, tissue necrosis leading to ulceration

Surgery is treatment of choice

Source = contaminated water

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Mycobacterium Leprae:

A

Chronic infectious disease
Very slow growing
Affects peripheral nerves, skin, and mucosa
Infects monocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Mycobacterium Leprae:

Transmission

A

person-to-person (very low rate of transmission) from nasal septa

Humans and armadillos only known natural hosts

95% of people who are exposed do NOT develop disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

Mycobacterium Leprae:

2 diseases?

A

Leprosy (Hansen’s Disease) - affects peripheral nerves, skin, mucosa

1) Lepromatous leprosy
2) Tuberculoid Leprosy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Lepromatous leprosy

A

malignant form, high bacterial numbers

Strong ab response, but defect in cell-mediated immunity

SX: loss of eyebrows, thick/enlarged nares, ears, and cheeks

Severe damage and loss of nasal bone/septa and sometimes digits

Skin and nerve involvement with loss of local sensation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

Tuberculoid Leprosy

A

self-limiting sometimes

Active cell-mediated immune response to lepromin

SX: blotchy red lesions on face, trunk, and extremities with loss of local sensation

87
Q

Isoniazid

Mechanism?
activation?
distribution?

A

prodrug, activated by TB catalase-peroxidase enzyme (KatG)

Inhibits mycolic acid synthesis in TB cell wall

Bactericidal in growing mycobacteria, bacteriostatic in resting organisms

Can penetrate caseous cavitary lesions - very good distribution

88
Q

Isoniazid

Mechanism of resistance

A

mutation or deletion of mycobacterial catalase-peroxidase KatG

89
Q

Isoniazid

Metabolism

A

Acetylated in liver → produces acetylhydrazine which is HEPATOTOXIC

90
Q

Isoniazid

Toxicity (5)

A

1) Hepatotoxic (“high acetylators”)
2) Peripheral neuropathy
3) Seizures
4) Depletes B6
5) Drug induced lupus (“slow acetylators”)

91
Q

Slow vs. fast acetylators and Isoniazid

A

Acetylated in liver → produces acetylhydrazine which is HEPATOTOXIC

**Increased risk in patients who are “slow acetylators” → increased risk of drug induced lupus
Increase risk of hepatotoxicity if you are a “fast acetylators” and thus producing more acetylhydralizine

92
Q

Rifampin

Mechanism

A

bactericidal (can enter cells) → effective against latent TB

Inhibits RNA polymerase initiation

Lipophilic → penetrates BBB

93
Q

Rifampin

Mechanism of resistance

A

rapid resistance if used alone - mutation of RNA pol

94
Q

Rifampin

Use (3)

A

TB treatment

H. influenzae prophylaxis

Meningococcal meningitis prophylaxis

95
Q

Rifampin

Toxicity

A

1) Inducer of CYP450 (induces metabolism of itself)
Rifabutin favored of rifampin in HIV patients because LESS CYP450 stimulation

2) Stains fluids and secretions red
3) Minor hepatotoxicity
4) Dizziness, visual disturbances, nausea, vomiting, diarrhea

96
Q

Ethambutol

Mechanism

A

inhibits carbohydrate polymerization of mycobacterium cell wall by blocking arabinosyltransferase

Tuberculostatic to TB, but can be -cidal for other mycobacteria

Not very good at entering cells

97
Q

Ethambutol (3)

A

optic neuropathy (reduced visual acuity, red-green color blindness, scotomas)

GI disturbance

decreased renal clearance of uric acid (gout)

98
Q

Pyrazinamide

Mechanism

A

Acts intracellularly in acidic pH of phagolysosomes where TB is found

Prodrug converted to active form pyrazinoic acid by pyrazinamidase enzyme

Readily crosses BBB

99
Q

Pyrazinamide

Mechanism of resistance

A

mutations in pncA gene and alterations in bacterial drug uptake

100
Q

Pyrazinamide

Toxicity

A

1) hepatotoxicity
2) hyperuricemia
3) GI intolerance
4) fever
5) acute intermittent porphyria

101
Q

Which three drugs are mycobacterial specific?

A

Isoniazid
Ethambutol
Pyrazinamid (?)

102
Q

Which drugs are tuberculocidal?

A

Isoniazid
Rifampin
Pyrazinamide
Streptomycin

103
Q

Which drugs are tuberculostatic?

A

Ethambutol

104
Q

Which TB drugs have good intracellular action? Which ones do not?

A

Intracellular = Isoniazid, Rifampin

Ethambutol (moderate intracellular activity)

Pyrazinamide = variable intracellular

Poor intracellular = streptomycin

105
Q

TB drug resistance

A

Monotherapy, inadequate drug regimen, or poor compliance all contribute to resistance. Can also acquire infection with a strain that is resistant

106
Q

MDR and XDR TB resistance

A

MDR = TB resistance to at least isoniazid and rifampin

XDR-TB = TB resistant to Isoniazid and Rifampin, plus any fluoroquinolone and at least one of three injectable second line drugs

107
Q

Treatment of TB - regimen?

A

1) Intensive phase (2 mo): isoniazid, rifampin, pyrazinamide, and ethambutol
2) Continuation phase (4-7 mo): Isoniazid, Rifampin

108
Q

Opportunistic Infection

A

an infection that occurs in a compromised host by an organism which does not usually infect a “normal” host

109
Q

Nosocomial infection

A

infections that occur in an institutional setting (hospital, convalescent centers, nursing homes)

110
Q

Iatrogenic infection

A

infections resulting from the activity of a physician or other healthcare giver

111
Q

Conditions that contribute to opportunistic infections: (5)

A

1) Granulocytopenia
2) Cellular immune dysfunction
3) Humoral immune dysfunction
4) Foreign Body
5) Surgery

112
Q

Conditions that contribute to opportunistic infections:

Granulocytopenia

predispose you to what bugs?

A

low PMNs from chemo or radiation therapy

→ Gram negatives and staph

113
Q

Conditions that contribute to opportunistic infections:

Cellular immune dysfunction

predispose you to what bugs?

A

AIDS, age, smoking, T-cell defects

→ Intracellular pathogens - Salmonella

→ Mycobacterium tuberculosis and avium, Listeria monocytogenes

114
Q

Conditions that contribute to opportunistic infections:

Humoral immune dysfunction

predispose you to what bugs?

A

Agammaglobulinemia, Splenectomy

Encapsulated pathogens → S. pneumoniae, Meningococci

115
Q

Conditions that contribute to opportunistic infections:

Foreign Body

predispose you to what bugs?

A

IV or urinary catheter, bone implant

Gram negatives, Staph

116
Q

Conditions that contribute to opportunistic infections:

predispose you to what bugs?

A

Staph, E. Coli, Pseudomonas

117
Q

3 mechanisms by which endotoxin (LPS) from gram negatives cause systemic disease?

A

1) Complement cascade activation → INFLAMMATION, high fever
2) Hageman Factor (XII) activation → Fibrinolysis, Hypotension
3) MACROPHAGES release TNF-a → activate factor 7 and 10 → DIC

118
Q

Pseudomonas Aeruginosa:

gram?
shape?
lactose?
oxidase?
catalase?
motility?
synthesizes what pigments?
A 
Gram negative bacilli
Non-lactose fermenting
Oxidase +
Catalase +
Motile
Synthesizes pyoverdin and pyocyanin
119
Q

pyoverdin and pyocyanin

A

Functions to generate ROS to kill competing microbes

→ sweet “grape-like” odor

120
Q

When grown on ___________ Pseudomonas generate a blue-green pigment

A

Grown on King’s A and B → Blue-green pigment

121
Q

Pseudomonas Aeruginosa

Virulence factors (4)

A

Exotoxin A

Phospholipase C: degrades plasma membrane

Pyocyanin: generates ROS

Endotoxin (LPS)

122
Q

Pseudomonas Aeruginosa

Exotoxin A mechanism

A

inhibits host protein production by ADP-ribosylation of EF2

123
Q

Pseudomonas Aeruginosa

Transmission

A

contact spread typically in immunocompromised patients (burn, nosocomial settings)

Widespread in moist areas of the environment and is part of normal gut flora in some people

124
Q

Pseudomonas Aeruginosa

Types of infections (7)

A

OPPORTUNISTIC PATHOGEN

1) Chronic pneumonia (especially CF and intubated patients)
2) Sepsis (burn and chemo patients)
3) Ecthyma gangrenosum: rapidly progressive, necrotic lesion) in immunocompromised patients
4) UTI
5) Otitis Externa
6) Osteomyelitis, Septic Arthritis → secondary to nail puncture wound to the foot
7) Skin infections (“hot tub folliculitis”, burn patients)

125
Q

Pseudomonas Aeruginosa

Resistance mechanisms:

A

High innate resistance mechanisms (many efflux pumps)

Propensity to form biofilms

126
Q

Iron and Bacterial Virulence:

Nearly all bacteria require iron for growth - which two bacteria are exceptions?

what happens if you have an excess of iron in your body (e.g. hemochromatosis)

A

Exceptions: Lactobacilli, Treponema pallidum

If a person has really high iron, they are more susceptible to infection!

127
Q

Challenges for bacteria with iron: (5)

A

1) Iron is poorly soluble under physiological conditions
2) Iron levels WITHIN bacteria varies 10x, while levels are highly variable outside bacteria
3) Most Fe2+ in humans is bound to transferrin or lactoferrin (only 20-30% saturated with Fe2+)
4) Excess iron is highly toxic to bacteria due to production of hydroxyl-radicals (Fenton reaction)
5) Host defences

128
Q

Host defenses and Iron (3)

A

Shunting of iron into storage during infection (liver)
Decrease iron absorption from intestine during infection
Decrease expression of microbial iron binding compounds

129
Q

Bacteria iron adaptations: (6)

A

1) Siderophores and high affinity uptake systems
2) Receptors to steal siderophores from normal flora bacteria
3) Reductase enzymes to free iron from host iron-binding systems
4) Receptors to bind host heme or lactoferrin and utilize their Fe directly
5) Microbial toxins to kill eukaryotic cells and release Fe
6) Proteases to degrade host iron binding proteins

130
Q

Sites of Viral Replication in the Respiratory Tract

-which virus prefers to replicate in the URT?

A

temperature differential between upper and lower respiratory tract → consequences for pathogenesis

Upper respiratory tract: preferential site for Rhinoviruses (exception is rhinovirus C)

The rest replicate in BOTH URT and LRT

131
Q

Patterns of viral infection:

3

A

1) Acute infection with replication confined to respiratory mucosal surface:
2) Persistent replication on respiratory mucosal surface:
3) Systemic replication after primary replication on respiratory mucosal surface:

132
Q

Acute infection with replication confined to respiratory mucosal surface: (4 viruses)

A

Paramyxovirus (parainfluenza)

Orthomyxovirus (Influenza)

Coronavirus

Picornavirus (rhinovirus)

133
Q

Persistent replication on respiratory mucosal surface:

3 viruses

A

EBV
adenovirus
papillomavirus

134
Q

Systemic replication after primary replication on respiratory mucosal surface: (6 viruses)

A 
Paramyxovirus (mumps, measles)
Varicella, Zoster, HHV6, CMV
Rubella
Picornavirus (poliovirus)
Poxviruses
Reoviruses
135
Q

Transmission of Respiratory Viruses

A

fomites, aerosol transmission

Primary interaction between respiratory viruses and host occurs at EPITHELIAL surface → infection of epithelial cells → release of cytokines → symptoms

136
Q

Influenza Virus

main features:

  • virus family
  • genome
  • shape, envelope
  • site of replication
A

orthomyxovirus

Helical, enveloped, negative segmented ssRNA

*NUCLEAR replication

Consist of Influenza A, B, and C

137
Q

Influenza A

A

animal species

Glycoproteins have greater variability than in strain B and C

HA undergoes minor and occasional MAJOR changes - very important = ANTIGENIC SHIFT

138
Q

Influenza B and C

A

human pathogens

B → relatively slow change in HA
C → uncommon strain

139
Q

Structure of Influenza virus

A

Envelope → bases for classification of influenza

Neuraminidase (NA)
Hemagglutinin (HA)

140
Q

Hemagglutinin (HA)

A

13 major antigenic types

Binds sialic acid on cells → facilitates endocytosis

141
Q

Neuraminidase (NA)

A

9 major antigenic types, enzymatic properties

Cleaves HA-sialic acid interaction during budding to permit viral spread

142
Q

Replication of Influenza virus?

what causes symptoms?

A

Virus replicates in ciliated epithelial cells of URT
→ Lysis and necrosis of cells

→ symptoms (fever, chills, muscular aching, headache, prostration, anorexia)

143
Q

Antigenic Drift

A

HA and NA drift occurs via POINT MUTATIONS

Minor antigenic changes that occur continuously in host populations during interpandemic periods due to selective advantage of new strain

Occur every year → slight alterations in HA or NA → EPIDEMICS

144
Q

Antigenic Shift

A

*ONLY Influenza A - radical change in HA and/or NA → emergence of new major antigenic variants due to GENETIC REASSORTMENT

Genetic reassortment occurs when more than 1 virus infects a cell

Exchange of RNA segments between human and animal virus → radically new HA or NA = PANDEMIC

145
Q

Influenza Prevention

A

Vaccines target A and B but NOT C

Seasonal flu vaccine (updated yearly): bivalent, protects against seasonal A and B influenza types

1) Attenuated (intranasal)
2) Killed virus

146
Q

Influenza Pathogenesis

A

spread primarily by aerosols
Can spread virus in absence of symptoms
Highly infectious, typically infection results in symptoms

Normally self-limited infection lasting 3-7 days

Death from primary influenza infection rare - usually due to secondary infection

147
Q

Why do people usually die from influenza?

what bugs (3) are often the cause of this deadly complication?

A

Death from primary influenza infection rare - usually due to secondary infection

Damage to respiratory epithelium predisposes to bacterial infections → deaths

Secondary bacterial pneumonia usually caused by:
Staph aureus
H. influenzae
Strep pneumoniae

148
Q

zanamivir, oseltamivir, peramivir

mechanism?

A

Neuraminidase inhibitors

149
Q

amantadine, rimantadine

A

High resistance to Amantadine

M2 channel blockers

150
Q

Parainfluenza virus

Main features

A

helical, enveloped capsid virus with negative sense ssRNA paramyxovirus

Envelope contains HA and NA

Contain viral fusion (F) surface proteins

151
Q

Parainfluenza virus

viral fusion (F) surface proteins - causes what?

A

causes infected cells to form multinucleated giant cells (syncytia) and mediates cell entry

152
Q

Parainfluenza virus

Transmission and Infection

A

Inhalation via aerosols → initial infection in larynx mucosa via HA and NA → progress down toward trachea and bronchial epithelium

→ Inflammation and swelling of mucous membranes → narrows lumen → can cause obstruction of inspiration and expiration

153
Q

Parainfluenza virus

Diseases (2)

A

1) Croup

2) Pneumonia

154
Q

Parainfluenza virus

Croup

A

(children): fever, hoarseness, barking cough upon expiration, inspiratory stridor

“Steeple sign” on XR (subglottic narrowing)

TX = glucocorticoids, nebulized epinephrine

155
Q

Measles (Rubeola) virus

Main feature

A

Paramyxovirus
Helical, enveloped capsid virus
Negative ssRNA

156
Q

Measles (Rubeola) virus

Matrix (M) Protein

A

regulates viral RNA synthesis and assembly

Strains that cause SSPE do NOT contain matrix (M) protein antigen

157
Q

Measles (Rubeola) virus

Replication

A

occurs during 8-10 day incubation period - measles virus replicates and lyses respiratory epithelial cells → infection and lysis of reticuloendothelial cells

158
Q

Measles (Rubeola) virus

Measles Disease

A

1) fever, malaise, anorexia
2) Conjunctivitis
3) Cough
4) Sore throat
5) Coryza (rhinitis)
6) Koplik’s spots
7) Rash

159
Q

Measles (Rubeola) virus

Koplik’s spots:

A

pathognomonic for measles

1-3 mm whitish/grayish/bluish elevations with erythematous base - seen on buccal mucosa near molar teeth

160
Q

Measles (Rubeola) virus

Rash of measles infection

A

maculopapular, blanching rash that appears days after prodrome phase

Begins on face, spreads centrifugally to involve body and extremities

RASH has NO ROLE in virus transmission

161
Q

Complications of Measles infection? (4)

A

1) Subacute Sclerosing Panencephalitis (SSPE)
2) Acute encephalitis (Rare)
3) Giant Cell Pneumonia (only in immunosuppressed)
4) Measles and pregnancy:

162
Q

Subacute Sclerosing Panencephalitis (SSPE)

A

Fatal, progressive degenerative disease of the central nervous system

Occurs 7-10 years after initial measles infection

Presentation: personality changes, lethargy, difficulty in school and odd behavior, progression to dementia, severe myoclonic jerking, flaccidity and decorticate rigidity

Strains that cause this do NOT contain matrix (M) protein antigen

163
Q

Measles and pregnancy

A

infection of pregnant women with MV can result in premature labor, spontaneous abortion, low-birth weight infants

164
Q

Measles prevention

A

live attenuated MMR vaccine

165
Q

Measles transmission and replication?

A

Transmission via respiratory droplets, is HIGHLY CONTAGIOUS

Replicates in nasopharynx and moves to lymph nodes → VIREMIA (5-7 days after exposure)

EXTENSIVE generalized virus infection in lymphoid tissue/skin

166
Q

Measles Histological examination signs:

A

Lymphoid organs show fused lymphocytes (Warthin Finkeldey Giant Cells) + paracortical hyperplasia

167
Q

Treatment of measles virus infection?

A

Treatment: supportive, can try Vitamin A

168
Q

Rubella

Main features

A

(not a respiratory virus): aka German Measles

icosahedral
enveloped
nonsegmented, positive sense ssRNA
Togavirus

169
Q

Rubella

Disease

A

German Measles aka “3 day measles”
Low grade fever and lymphadenopathy 1-5 days prior to rash
RASH

170
Q

Rubella

Characteristic rash?

A

maculopapular rash, begins on face, spreads to extremities

Antibody mediated

Present for 3 days

171
Q

Pregnancy and Rubella:

Manifestations in women

A

Women infected get postauricular and occipital lymphadenopathy with maculopapular rash

172
Q

Congenital rubella

A

occurs with infection during FIRST trimester

PDA, cataracts, sensorineural deafness

Pulmonary artery hypoplasia

Microcephaly

Purpuric “blueberry muffin” rash (dermal erythropoiesis)

173
Q

Rubella

Prevention

A

MMR live-attenuated vaccine

174
Q

Rubella

Transmission

A

aerosol droplets or transplacentally

Aerosol infection of nasopharynx → 14-21 day incubation period with replication in local lymph nodes → prodrome

175
Q

Mumps

Main Features:

A

Paramyxovirus
Helical, enveloped capsid virus
Negative ssRNA

176
Q

Mumps

Structure

A

Fusion (F) surface protein

causes infected cells to form multinucleated giant cells (syncytia)

177
Q

Mumps

Prevention

A

MMR live attenuated vaccine → immunity for life

178
Q

Mumps

Tranmission

A

Transmission via respiratory droplets

Humans are ONLY natural reservoir

Less infectious than measles and chickenpox

179
Q

Mumps

invasion and replication

A

Invades URT epithelium via hemagglutinin envelope proteins → local lymph nodes → VIREMIA

2-3 week incubation period → inflammation and edema of glandular tissue, spread to meninges

180
Q

Mumps Disease

A

Parotitis → elevated serum amylase, leukopenia, lymphocytosis

Orchitis

Meningitis (aseptic) and encephalitis

Acute pancreatitis

181
Q

Mumps - treatment?

A

supportive

182
Q

RSV

Main features?

A

Paramyxovirus

Helical, enveloped capsid virus

Negative sense ssRNA

183
Q

RSV

Structure (2 main proteins and their function)

A

Viral fusion (F) protein → infected cells fuse and form syncytia

Protein G → allow attachment to bronchiolar and alveolar epithelium → necrosis and inflammation of bronchioles and alveoli

184
Q

RSV

Disease

A

Lower respiratory tract disease (Infant Bronchiolitis, Pneumonia)

One of the most common causes of pneumonia in children and bronchiolitis (especially children)

→ Affects many children UNDER 6 months of age

Can cause bronchitis, pneumonia, and croup

185
Q

RSV

Diagnosis (3 ways)

A
  • epidemiology
  • nasal swab tests to detect RSV antigen
  • histology of cells from LRT
186
Q

RSV - Prevention

1 drug and its mechanism/use

A 
Palivizumab: monoclonal antibody used for prophylaxis in immunocompromised at high risk for RSV
Targets F (fusion) protein of RSV → inhibit cell entry
187
Q

RSV transmission

A

Transmission via respiratory droplets

188
Q

RSV treatment - 1 drug and its mechanism/use

A

Ribavirin: purine nucleoside analog

Used in severe cases of RSV in immunocompromised patients

189
Q

Orthomyxoviruses

  • viruses that belong to this family?
  • replication?
  • genome?
  • envelope?
A

Influenza: A, B, and C

Nuclear replication
Segmented (-) sense RNA

Enveloped

190
Q

Paramyxoviruses

viruses that belong to this family?

A

Paramyxovirus: Mumps, Parainfluenza

Morbillivirus: Measles

Pneumovirus: RSV

191
Q

Paramyxoviruses

  • replication?
  • genome?
  • envelope?
A

Cytoplasmic replication

No polarity to their infection (can come in/go out both apical or basal side)

Non-segmented (-) sense RNA

LITTLE genetic variation

Enveloped

192
Q

How do the glycoproteins on paramyxoviruses differ from those on orthomyxoviruses

A

Glycoproteins: do not form such prominent spikes as on influenza virus
HN - Hemagglutinin + Neuraminidase activities
Measles → H protein (no neuraminidase activity)
RSV → G protein (neither activity

193
Q

Virus cultivation (2 ways we do this)

A

1) growth in tissue culture cells

2) cytopathic effects (CPE)

194
Q

Growth in tissue culture cells:

3 steps

A

1) Cells in culture → add patients sample to cells → cells will become infected if patient is infected
2) Anti-virus Ab added → binds infected cells
3) Fluorophore-labeled anti-IgG Ab → lights up if present

195
Q

Cytopathic effects

A

provides evidence of presence of infectious virus

196
Q

Tests for virus antigen - 4 tests that do this

A

1) Western blot
2) immunofluorescence assay
3) hemadsorption
4) rapid immunoassays

197
Q

Hemadsorption

what does it test?
how do tests results differ for infected vs. uninfected cells?

A

Tissue culture cells + RBCs

Uninfected → No RBC binding (Hemadsorption negative)

Infected → RBC binding to infected tissue culture cells (Hemadsorption positive)

-tests for virus antigen

198
Q

Tests for virus nucleic acid

3 tests that do this

A

PCR
RT-PCR
Multiplex PCR (qualitative vs. quantitative)

199
Q

RT-PCR

4 steps

A

Reverse Transcription PCR

1) viral ssRNA reverse transcribed into cDNA
2) cDNA/RNA hybrid then melted to separate RNA and cDNA
3) Add specific viral primer + DNA polymerase → synthesis of second strand cDNA
4) dsDNA melted and amplified for detection → run on gel and look for dsDNA of a specific size

200
Q

What does RT PCR look for?

what is it used to screen?

A

*used to screen donated blood for virus

Tests for virus nucleic acid

201
Q

Tests for virus-specific antibody

A

1) ELISA
2) Virus-Specific IgM or IgG Capture ELISA
3) Western blot
4) Hemagglutination Inhibition
5) Hemadsorption Inhibition Test

202
Q

ELISA

3 steps
what does it test for?

A

1) Each well coated with virus antigen → patient sample added to well (may or may not contain Abs specific for antigen in well)
2) Enzyme linked anti-human IgM or IgG added to well
3) Add enzyme substrate - if enzyme present, will produce color change

Tests for virus-specific antibody

203
Q

Virus-Specific IgM or IgG Capture ELISA

A

1) Each well coated with anti-human IgM or IgG
2) Add patient sample, all IgM (or IgG) Abs bound in well
3) Virus antigen added
4) Enzyme linked anti-virus antigen Ab added to well
5) Add enzyme substrate → color change if enzyme present

204
Q

Hemadsorption Inhibition Test

  • test results for infected vs. non-infected
  • tests for what?
A

Infected cells in tissue culture + RBCs → RBC binding to viral surface protein

Infected cells + RBCs + Abs to cells (specific for specific viral proteins)→ NO RBC binding because specific antibodies have blocked RBC binding

CONFIRMS infection via a specific virus

Do NOT know that this virus is the cause of the patient’s illness

205
Q

Hemagglutination Inhibition Test

A

serological confirmation that isolated virus was associated with patient’s disease

tests for virus specific antibody

206
Q

Hemagglutination Inhibition Test

test results for infected vs. non-infected

A

RBCs + virus → Hemagglutination (network formation)
-When hemagglutination occurs that shows there are NO antiviral antibodies present in the patient’s serum (aka not cause of patient’s disease)

RBCs + virus + Ab → No hemagglutination (Ab binds virus, prevents RBC binding with virus)

207
Q

Adenoviruses

main features

A

linear dsDNA virus, icosahedral, non-enveloped

  • Very common, most are asymptomatic
  • Different serotypes associated with different diseases
  • Can be reactivated during immunosuppression (AIDS)
  • Virus can shed for long periods after infection, asymptomatic
208
Q

Adenoviruses

Mode of entry and replication

A

virus binds via hemagglutinin and enters and lyses mucosal cells

209
Q

Adenoviruses

Diseases (7)

A

Acute respiratory disease and pneumonia

  • Conjunctivitis
  • Common cold

Acute hemorrhagic cystitis

Gastroenteritis (day care - not as common as rotavirus)

Myocarditis

More serious clinically in immunosuppressed)

210
Q

Rhinovirus

main features

A

picornavirus family

Linear positive sense ssRNA virus, naked, icosahedral capsid

211
Q

Rhinovirus

Mode of entry and replication

A

Binds ICAM-1 of URT epithelial cells → spreads locally WITHOUT killing cells → local inflammation, increase ICAM-1 expression

Acid LABILE (does not cause GI disease)

Preferentially replicates at cooler temp (33 C) in nose/upper airways

212
Q

Rhinovirus

Diseases (3)

A

1) Most common cause of URT (e.g. “cold”)
- Generally self-limiting

2) Otitis media
3) Exacerbations of chronic pulmonary disease

213
Q

Coronavirus

main features

A

Large +ssRNA, enveloped, non segmented, helical capsule

Unstable in environment

214
Q

Coronavirus

Diseases (3)

A

Can cause systemic disease

1) Common cold (second most common cause)
2) Severe acute respiratory syndrome (SARS)
3) Middle East Respiratory Syndrome (MERS)

Infectious Disease (9 decks)

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