Brainscape's Knowledge GenomeTM

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


See full index

BIOM 360 > Exam 3 Chapter 39 > Flashcards

Exam 3 Chapter 39 Flashcards

1
Q

What makes up the Chain of Infection?

A

Agent, Virulence, Exposure, Dose, Susceptibility

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

What is the Agent in the Chain of Infection?

A

Agent - pathogen, bug that could cause us trouble

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

What is the virulence in the Chain of Infection?

A

Magnitude of harm it can do to its host

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

What is the Exposure in the Chain of Infection?

A

Pathogen transmission

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

What is the Dose in the Chain of Infection?

A

Dose = Initial innoculum to the host

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

What is the susceptibility in the Chain of Infection?

A

ability of the host to fight the pathogen or pathogens

(can look at immune system status, pathogenosity or virulence of the bug, host nutrision, host stress level)

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

Name and describe the stages in the course of infection and disease

A

Incubation period = period where the intensity of symptoms is zero and the initial exposure of microbe

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

What is the prodromal stage in the course of infection and disease?

A

Initially start to feel bad, host is contagious

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

What is the period of invasion course of infection and disease?

A

Time where you have the symptoms and signs you have the disease

Height of infection

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

What is the convalescent period?

A

getting better and decreasing the intensity of symptoms

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

What happens if there is a height of infection and your body cannot fight it off anymore?

A

Death

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

What bacteria causes Chlamydial Pneumonia?

A

Chlamydophila pneumoniae

Gram Negative coccoid

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

How is Chlamydial pneumoniae transmitted?

A

Airborne Routes

elementary bodies infect, reticulary bodies repliate

Non sexually transmitted

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

What are elementary bodies?

A

Infect new hosts

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

What are reticular bodies?

A
  • metabolically inactive except passing pathogen on, once inside host
  • Are metabolically active, but non infectious. Need to convert back to elementary bodies to infect
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the clinical manifestations of Chlamydophila pneumoniae bacteria?

A

fever, productive caugh, and mild pharyngitis, bronchitis, and sinusitis

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

Describe the diagnosis, treatement and prevention for Chlamydophila pneumoniae?

A
  • observation of symptoms and a microimmunofluorescence test (infect with fluorescent antibodies)
  • Antibiotic therapy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are macrolyte?

A

affect 50S ribosomal that inhibits protein synthesis

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

What are the common airborne bacterial diseases?

A
  • Chlamydial pneumonia
  • Diphtheria - Exotoxin Mechanism
  • Legionnaires’ Disease
  • Meningitis
  • Mycobacterium Infections (M. avium complex = MAC)
  • Tuberculosis (TB)
  • Mycoplasmal pneumonia
  • Pertussis
  • Streptococcal Diseases (Streptococcal pharyngitis)
  • Post-streptococcal Diseases (Glomerulonephritis = Bright’s disease and rheumatic fever)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What bacterium is Diphtheria caused by?

A

Corynebacterium diphtheriae

= Gram positive bacilli

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

What are varialence factors?

A

Help the camofage and make it so human cells do not recognize as a disease

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

Explain how Diphtheria works?

A

Lysogenized strains of Diphtheria produce an exotoxin that inhibits protein synthesis and is responsible for pathogenesis

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

What is Diphtheria resistant to?

A

Resistant to drying

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

How is Diphtheria transmitted by?

A

Airborne transmission by nasopharyngeal (NP) secretions - crwding increase likelihood of transmission

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

What age group is Diphtheria observed in?

A

Usually observed in individuals > 30 years old with weakened immunity to diphtheria toxin and living in tropical areas

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

What is cutaneous diphtheria?

A
  • infection at woonds or skin lesion
  • Slow- healing ulceration (tend to look gray when healing due to pseudomembrane)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

How does one diagnose Diphtheria?

A

Pseudomembrane in throat or bacterial culture

(throat cultures can cause it to dislodge and block airway)

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

What is the treatment for Diphtheria?

A

– Antitoxin neutralizes unabsorbed exotoxin in patient’s tissues

– antibiotic therapy

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

What else can Diphtheria invade?

A

Can invade circulatory system, cardiac, kidney, nervous system and inhibit protein synthesis in that area

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

What is the prevention of Diphtheria?

A

The main prevention is mainly vaccinations:

  • the diphtheria/tetanus/pretussis vaccine to children (DTap)
  • Non-immunized adolescents and adults (Tdap)
  • Booster in adolescents and adult is the diphtheria/tetanus vaccine (Td) every 10 years

Schedule:

  1. DTap at 2, 4 and 6 months of age
  2. booster at 12-18 months
  3. Booster at 4 - 6 years
  4. Tdap vaccine at 11 - 12 years
  5. Booster of Td at 10 years
  6. Tdap vaccine during second half of each pregnancy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What bacteria is responsible for Legionnaire’s Disease?

A

Legionella pneumophila

fastidious, Gram - Negative = rod shaped

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

How is Legionella pneumophila harbored?

A

by free-living amoebae and ciliated protozoa

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

How is Legionnaires’ Disease spread?

A

Airborne transmission from environmental reservoir to human host

*Soil, aquatic ecosystems, air-conditioning systems and shower stalls (LOVE WATER)

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

What has Legionella been known to cause?

A

Can cause an inflammatory reaction (pneumonia) in the lungs called legionellosis

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

What causes localized tissue destruction with Legionellosis?

A

Reproduction of bacterium in alveolar macrophages

  • Hits the lungs
  • Produce cytotoxic exoprotease = (produce a distructive enzyme to breakdown lungs)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What are the clinical manifestations of Legionnaires’ Disease?

A
  • Fever, cough, headache, neuralgia (muscle pain), and bronchopneumonia
  • Serve in immunocompromised people/elderly
  • Pontiac fever: nonpneumonic form, flu- like symptoms, resolves by itself (less severe)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What is the treatment, prevention and control for Legionnaires’ Disease?

A
  • Isolation of bacteria and immunodiagnostics
  • Symptomatic/supportive therapy and antibiotic therapy
  • Eliminate nosocomial spread (if we have large amount of people, break groups up)
  • Identification/elimination of environmental source
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What symptoms does meningitis cause?

A

Inflammation of brain or spinal cord meninges (membranes)

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

What are the causes of the Meningitis?

A
  • Bacterial and viral = most common but can get fungal or parasite
  • Bacterial may be diagnosed by gram stain of cerebrospinal fluid (CSF)
  • culture of CSF may or may not grow bacteria
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What are the major bacterial causes of Meningitis?

A
  1. Streptococcus pneumoniae
  2. Neisseria meningitidis (sterotypes)
  3. Haemophilus influenza (serotype b)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Which of the three bacterial causes of Meningitis is most common in 5 year and younger individuals?

  1. Streptococcus pneumoniae
  2. Neisseria meningitidis (sterotypes)
  3. Haemophilus influenza (serotype b)
A
  1. Haemophilus influenza (serotype b)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What does N. meningitidis (meningococcus) cause?

A

Epidemic meningitis

(mainly upper respiratory system therefore can get into spinal cord)

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

How is Meningitis transmitted?

A

Respiratory droplets

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

What are the clinical manifestations of Meningitis?

A
  • Initial respiratory illness or sore throat interrupted by one of the following:
    1. Vomiting, headache, lethargy, confusion, and stiffness in neck and back

(There is viral meningitis and not much treatment but the bacterial version is the most concerning strain)

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

What is the clinical manifestation of Aseptic Meningitis Syndrome?

A

Similar to bacterial meningitis but show no microbial agent in gram-stained specimen and in culture

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

What is the treatment, prevention and control of Meningitis?

A
  • Must rule out bacterial diagnosis
  • Treatment difficult
    1. S. pneumoniae
  • Vaccine and antibiotics
    2. N. meningitidis
  • Antibiotics (also prophylactic), vaccine
  • recommended for college students, others
    3. H. influenzae
  • pneumonia and meningitis kill 3 million worldwide/year
  • Vaccine (Hib) reduced cases to 1/100,000
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Where is Mycobacterium bacteria found in?

A

Soil, water and house dust

one of the oldest documented diseases

Grows very slowly and people do not know they have something and have an unusal cell wall = acid fast (special stain)

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

Why is Mycobacterium Infections difficult to treat?

A
  • mycolic acid in cell wall is protective waxy material that is acid fast (will stain a faint blue)
  • Resistant to penetration of some antibiotics (rice shaped)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What is mycobacterium infections referred to as?

A

M. avium complex (MAC)

  • normal inhabitants of soil and water
  • Infect variety of insects, birds, and other animals
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What is the portal of entry for the Mycobacterium Infection?

A

Respiratory and gastrointestinal tracts

  • Most common cause of mycobacterial infections in the U.S.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What are the clinical manifestations for M. avium complex (MAC)? (Mycobacterium infection)

A
  1. pulmonary infection (similar to tuberculosis)
    - Usually observed in elderly patients with preexisting pulmonary disease
  2. Gastrointestinal infection
    - Common in AIDS patients
    - fever, malaise, weight loss, and diarrhea
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What is the treatment, prevention, and control of M. avium complex (MAC)? (Mycobacterium Infections)

A
  • Isolation from sputum, blood, or bone marrow (variety of samples - for sputum - 3 samples)
  • Acid-fast strain, and immunodiagnostic tests (changes in antibody levels)
  • multiple drug therapy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What is the bacteria that causes Tuberculosis (TB)?

A

Mycobacterium tuberculosis (Mtb), M. bovis, M. africanum

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

What is the important facts to know about Tuberculosis (TB)?

A
  • ~1/3 world’s population infected
  • worldwide distribution
  • many are also HIV positive (over 50% of TB deaths worldwide are in AIDS patients)
  • U.S. elderly, homeless, alcoholics, prisoners, and immigrants are some commonly infected groups
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What is the transmission of Tuberculosis (TB)?

A
  • Majority is person to person spread of droplet nuclei in respratory tract
  • Also transmitted from infected animals and their products
  • Reactivation of old, dormant infections
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Explain the speed that the Tuberculosis (TB) develops?

A

Disease develops slowely

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

What are the virulence factors for Tuberculosis (TB)?

A

Unique toxic cell envelope components (Unique lipids and glycolipids that make toxins that kill the host cell and survive phagocytosis because of this)

  • Mycolic acid, lipoarabinomannan, trehalose dimycolate, phthiocerol dimycocerosate
  • Kill eukaryotic cells and protect the bacterium from lysozyme and osmotic lysis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

How does Tuberculosis survive phagocytosis?

A
  1. Kill macrophages
  2. resistant to oxidative killing
  3. Inhibit diffusion of lysosomal enzymes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Explain the course of the tuberculosis (TB) disease and how it survives

A
  • Lung macrophages that have phagocytosed M. tuberculosis often die in the attempt to kill the bacteria
  • Survives by forming tubercles:
  • Composed of bacteria, macrophages, T cells and human proteins
  • Subsequent changes in tubercle may occur
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

When viewing on a skin or x-ray test, how does primary tuberculosis show up?

A

Skin -

X ray -

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

When viewing on a skin or x-ray test, how does delayed-type hypersensitivity and cell-mediated immunity tuberculosis show up?

A

Skin +

X ray -

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

Name and describe the stages of primary tuberculoses. Skin and X ray test results?

A

1. Disseminated tuberculosis (Skin -, X ray +)

A direct extension of primary tuberculosis. Spread throughout the body.

2. Latent-dormant tuberculosis (Skin +, X ray -)

The usual outcome. Most persons remain in this condition for life and suffer no ill effets. (activates after many years to then go into Active tuberculosis stage)

3. Active tuberculosis (skin +, X ray +, sputum +)

A slow progressive extensition of tuberculosis with erosion into the air passages and blood vessels. Death if not treated

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

What is the basis for the tuberculin (TB) skin test?

A

Develop cell-mediated immunity (sensitized T cells)

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

What is the incubation period for TB infection?

A

4-12 weeks

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

What are the symptoms of TB infection?

A
  • Fever, fatigue, weight loss
  • Cough: Characteristic of pulmonary involvement, many result in expectoration of bloody sputum (coughing up blood)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

How are the ways that TB is diagnosed?

A
  • Observation of acid-fast bacteria
  • Chest X-ray, Mantoux, or tuberculin skin test
  • DNA -based tests
  • QuantiFERON TB gold (brand new-blood test drawn in 3 tubes, advantage = saves patient from coming back in to see if they react to skin test)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

What is the antimicrobial theroapy for TB?

A
  • Multi-drug-resistant strain (MDR-TB)
  • Extensively drug resistant strains (XDR-TB)
  • Resistance develops due to naturally occuring chromosomal mutations and natural selection of resistant Mrb due to lack of adherence to tratement protocol
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

What is the prevention and control of TB?

A
  • Rapid, specific therapy to interrupt spread, retreatment of patients with MDR-TB, immunization, improved sanitation and housing, and reduction in homelessness and drug abuse
  • Directly observed therapy (DOTS)
  • antibiotics for 6-9 months
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q
A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What is the bacteria that causes Mycoplasmal Pneumonia?

A

Mycoplasma pneumonia

causes atypical pneumonia as opposed to consistent signs and sumptoms of typical pneumonia

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

How is Mycoplasmal Pneumonia transmitted?

A

By close contact and airborne droplets

Worldwide distribution

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

Explain the structure of M. pneumoniae

A
  • lacks cell wall
  • Resistant to beta-lactam antibiotics
  • attach to lower respiratory tract cells
  • produces peroxide, which may be toxic factors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Explain the clinical manifestation for Mycoplasmal pneumonia

A
  • Mild in infants and more serious in older children and young adults
  • headache, weakness, low fever, charactereistic cough, and pneumonia that presists for weeks
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Explain the diagnosis for Mycoplasmal pneumonia

A
  • Rapid immunological tests
  • Isolation from respiratory secreations -> “Fried egg” appearance of organisms on agar
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

What is the treatment, prevention and control for Mycoplasmal Pneumonia?

A
  • Likely cause when other bacteria and virsuses cannot be detected and immunodiagnostic tests
  • Antibiotic therapy
  • No preventitive measures
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

What is another name for Pertussis?

A

Whooping cough

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

What is the bacteria that causes Pertussis?

A

i.e. Whooping cough

= Bordetella pertussis

(gram negative bacilli or coccobacilli)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Explain the transmission of Pertussis

A

ie Whooping cough

  • Highly contagious disease that primarily affects children
  • Transmission by droplet inhalation
  • can be recovered from dried mucus for up to 3 days
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

Explain the toxins of Pertussis

A

i. e. Whooping Cough
- Toxins cause nitric oxide production:

1. pertussis toxin = most important toxin - stops protein synthesis

2. tracheal cytotoxin = dermonecrotic toxin - destroys epithelial tissue

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

How long is the incubation period for Pertussis

A

i.e. Whooping cough

Incubation period is typically 7-10 days but may range from 5-21 days and as long as 41 days

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

What is the infectious period for Pertussis for:

  1. Adolescents and adults
  2. Infants
A
  1. Adolescents and adults are infectious until 21 days after onset of paroxysmal cough
  2. Untreated infants may remain infectious for 6 weeks or longer
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

What are the clinical manifestations for Pertussis?

A
  • 7 to 14 day incubation
  • Initial cold- like symptoms/ inflamed mucous membranes
  • followed by prolonged coughing sieges with inspiratory whoop
  • permanent or long- lasting immunity develops
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

What is the treatment, prevention and control of Pertussis?

A
  • Bacterial culture, fluorescent antibody staining, and serological tests
  • Antibiotic therapy
  • Immunization with DPT for younger or Tdap acellular vaccines for older children and adults
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

What is the bacteria that causes Streptococcal Diseases?

A

Streptococcus pyogenes

Gram positive cocci

  • one of the most important pathogens

group A beta-hemolytic streptococci (GAS)

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

What are the virulence factors for Streptococcus pyogenes?

A
  • Extracellular enzymes that break down host molecules
  • Streptokinases - dissolve clots
  • Streptolysin O and S - kill host leukocytes (defense)
  • capsules and M proteins for attachment
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

What is the transmission for Streptococcal diseases?

A

Respiratory droplets, direct or indirect contact

widely distributed, some carriers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

How is Streptococcal diseases (streptococcus pyogenes) diagnosed?

A
  • Based on clinical laboratory findings
  • Rapid diagnostic tests available
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

What does the M protein of Streptococcus pyogenes look like?

A

Hair pins- hold in place

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

What is the common infection strep throat called, how is it spread and where does it infect?

A
  • Called = Streptococcal pharyngitis
  • Spread = by droplets of saliva or sasal secreations
  • Infection = in throat (pharyngitis) or tonsils (tonsillitis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

What are the symptoms of streptococcal pharyngitis?

A

i. e. Strep throat
- Symptoms of disease not diagnostic becasue many viral infections have similar presentation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

What are the physical manifestations of streptococcal pharyngitis?

A

i. e. Strep throat
- redness, edema, exudate and lymph node enlargement in throat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

How is streptococcal pharyngitis diagnosed?

A

rapid kits

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

How is streptococcal pharyngitis treated and controlled?

A
  • Antibiotics important for childred to lessen chance of complications (rheumatic fever and glomerulonephritis)
  • control by preventing contact with contaminated material or infected individuals
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

What are post-streptococcal diseases?

A

Glomerulonephritis (Bright’s disease) and rheumatic fever

Nonsupportive (nonpus-producing)

Most serious problems associated with streptococcal infections in U.S.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

When do Post-streptococcal diseases come on?

A

1-4 weeks after an acute streptococcal infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

What is Glomerulonephritis?

A

Inflammatory disease of renal glomeruli (a type III hypersensitivity)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

What are the clinical manifestations of Glomerulonephritis?

A
  • edema, fever, hypertension, and hematuria
  • may spontaneously heal or may become chronic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

What is the diagnosis of Glomerulonephritis?

A

clinical history, physical findings, and confirmatory evidence of prior streptococcal infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

What is the treatment for Glomerulonephritis?

A

antibiotic therapy (to kill residual bacteria), otherwise no specific therapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

What is the Autoimmune disease involving heart valves, joints, subcutaneous tissues and central nervous system?

A

Rheumatic Fever

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

What are the clinical manifestations for Rheumatic Fever?

A

vary widely, making diagnosis difficult

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

What is the treatment, prevention and control of Rheumatic Fever?

A
  • therapy directed at decreasing inflammation and fever, and controlling cardiac failure
  • treatment with salicylates and corticosteroids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

What are Arthropods?

A
  • Indirectly harm–transmit… not produce
  • some are true parasites
  • some inflict direct harm via bites, stings, or other activities
  • can carry more than one type of pathogen
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

Explain Arthropod-Borne Diseases

A
  • Generally rare
  • Some are of historical interest (such as plaque and typhus)
  • Some newly emerged (such as Lyme disease and erlichiosis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

What is the bacteria for Lyme disease?

A
  • LD or Lyme borreliosis
  • Most common tick-borne disease in the U.S
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

What is lyme disease caused by in the US and Europe and Asia (most common)?

A
  • Borrelia burgdorferi = U.S
  • B. garinii and B. afzelii = Europe and Asia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

How is Lyme disease transmitted?

A
  • From animal reservoirs by ticks (lxodes scapularis and I. pacificus)
  • deer, field mice and woodrats
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

What are the clinical manifestations and stagest of Lyme disease?

A
  • Clinical manifestations vary with three stages of disease:

- Initial (localized stage) : develops 1 week to 10 days after infection with an expanding, ring-shaped skin lesion with flu-like symptoms

- Disseminated : Occurs weeks or months after infection with neurological abnormalities, heart inflammation and arthritis (lyme arthritis may be autoimmune to joint MHC which are similar to bacterial antigens)

- Late Stage : occurs years later and has demyelination of neurons, behavioral changes and symptims resembling Alzheimer’s disease and multiple sclerosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

What are the two families of ticks that cause Lyme disease? how do they differ?

A
  1. hard ticks = ixodidae
  2. soft ticks - argasidae
    - Differ by feeding habits. Soft ticks complete their meals in a matter of minutes or a few hours. Hard ticks feed slowly, taking up to 7-9 days
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

How is Lyme disease diagnosed?

A
  • serogical testing (Lyme ELISA or Western blot)
  • Isolation of spirochete from patient
  • Detection of Borrelia DNA (PCR)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

How is Lyme disease treated, prevented and controlled?

A
  • Antibiotic therapy most effective in early stages
  • tick control and avoiding ticks
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

What is the bacteria that causes Plague? (G+ or G-)

A

Yersinia pestis - gram negative

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

How is plague transmitted?

A
  • rodent to human
  • bite of infected flea, direct contact with infected animal or product, inhalation contaminated air borne droplets
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

What happens once the Plague gets into the body?

A
  • multiply in blood and lymph
  • survive and proliferate in phagocytic cells
  • enlarge lymph nodes (buboes)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

Explain the plague infectious cycle

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

What are the virulence factors for Plague?

A
  • proliferates in phagocytes, not killed
  • Type III secretion systems deliver yersinal outer membrane proeins (YOPS) into cells which shut down defense mechanisms
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

What is the select agent for plague?

A
  • Y. pestis
  • potential bioterrorism threat
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

What are the clinical manifestateions for plague?

A
  • subcutaneous hemorrhages, fever, and buboes (hence name bubonic plague)
  • High mortality if untreated
  • Pneumonic plague arises from
  • primary exposure to infectious respiratory droplets of infeted persons or cats
  • secondary to hematogenous spread in a patient with bubonic plague
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

What is the diagnosis of plague?

A

Diagnosis made in reference labs which use direct microscopic examinations, cultures and serological tests and PCR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

What is the treatement, prevention and control for plague?

A
  • antibiotic therapy
  • Ectoparasite and rodent control, isolation of human patients, prophylaxis of exposed persons, immunization of persons at high risk
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

What is the cause of Rocky Mountain Spotted Fever?

A
  • Rickettsia rickettsii
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

How is Rocky Mountain spotted fever transmitted?

A

By ticks!!!

  • Transovarian passage - transmission of bacteria from generation to generation of ticks through their eggs
  • Passage by tick feeding or by defectation of tick and rubbed into skin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

How is Rocky Mountain Spotted Fever reproduced?

A

in epithelial cells and macrophages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
124
Q

What is located on tissue? what is located in blood stream?

A

Macrophage = on tissues

Monocyte = blood stream (largest)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
125
Q

What are the clinical manifestations of Rocky Mountain Spotted Fever?

A
  • Vasculitis and sudden onset of headache, high fever, chills and skin rash
  • Can destory blood vessels in heart, lungs or kidneys, leading to death
126
Q

How is Rocky Mountain Spotted Fever diagnosed?

A

observation of signs and symptoms and serological tests

(sends patient into DIC - throwing clots - deceminated intravascular coagulation)

127
Q

How is Rocky Mountain Spotted Fever treated, prevented and controlled?

A
  • antibiotic therapy and symptomatic/supportive therapy
  • tick control and avoidance of ticks
128
Q

Is it possible for arthropods to carry more than 1 type of pathogen?

A

YES

129
Q

What is direct contact dieseases? explain

A
  • Most involve skin or underlying tissues
  • some can become disseminated
130
Q

What is Gas Gargrene caused by?

A

or called Clostridial Myonecrosis

  • Caused by: Clostridium perfringes
  • Gram positive, spore- forming rod
  • Secretes toxin and tissue damaging enzymes
131
Q

What does gas gangrene infect?

A

a necrotizing infection of skeletal muscle or clostridial myonecrosis

132
Q

How is Gas Gangrene transmitted?

A

by contamination of injured tissue by spores from soil or bowel microbiota

133
Q

What are the clinical manifestations of Gas Gangrene?

A
  • severe pain, edema, drainage, muscle necrosis
134
Q

How is Gas Gangrene diagnosed?

A

recovery of appropriate clostridial species and characteristic disease symptoms

135
Q

What is the treatment, prevention and control of Gas Gangrene?

A
  • surgical debridement, administration of antitoxin, antibiotic therapy and hyperbaric oxygen therapy
  • Prompt treatment of all wound infections and amputation of limbs
136
Q

How is Group B streptococcal disease cause? bacteria?

A

Streptococcus agalactiae or group B streptococcus (GBS)

Gram Positive

137
Q

What does group B streptococcal disease cause for neonatal and newborns?

A
  • sepsis, meningitis and pneumonia
138
Q

How is group B Streptococcal disease transmitted?

A

Directly from person to person with many people being transient carriers

  • vagina may be source for newborns
139
Q

What are the clinical manifestations for Group B streptococcal disease?

A
  • Early onset disease
  • Presents within first few hours after birth
  • may be severe meningitis or death
  • Late onset disease - rare
140
Q

What is teh diagnosis for Group B streptococcal disease?

A

Gram Positive, beta - hemolytic, streptococcal bacteria growth from cultures of otherwise sterile body fluids

141
Q

What is the treatment, prevention and control for Group B streptococcal disease?

A
  • detect pregnant carriers
  • antibiotics
142
Q

What are mycobacterial skin infections?

A
  • Leprosy
  • Tattoo- associated Mycobacterial Infections
143
Q

What is another name for Leprosy? where is it most commonly found?

A

Hansen’s disease, most common in tropics

144
Q

What is Leprosy caused by and how is it invading?

A

Mycobacterium leprae

  • invades peripheral nerve and skin cells, becoming obligate intracellular parasites
145
Q

How is Leprosy transmitted and spread?

A

Humans are only significant reservoir (obligate intracellular parasite)

  • Transmitted after prolonged exposure to infected individual
  • probably spread in nasal secretions
146
Q

What are the clinical manifestations of Leprosy?

A
  • Incubation usually 3 to 5 years
  • initial symptoms is slightly pigmneted skin eruption
  • development of disease throught to be related to strength of cell0mediated immune response to bacterium
147
Q

What are two common forms of Leprosy (describe)

A

Tuberculosis (neutral) leprosy

  • Mild, nonprogressive form
  • associated with delaying-type hypersenstivity
  • damaged nerves and regions of skin surrounded by a border of nodules

Lepromatous (progressive) leprosy

  • Individuals do not develop hypersensitivity
  • skin tissue killed, leading to progressive loss of facial features, fingers, toes
  • disfiguring nodules form on body
148
Q

What is the diagnosis for Leprosy?

A

direct fluroescent antibody staining of biopsy specimens, serodiagnostic tests, DNA amplification and ELISA (more difficult to stain so cannot just do gram staining)

149
Q

What is the treatment prevention and control for Leprosy?

A
  • Long term antibiotic and drug therapy, and immunotherapy with vaccine
  • identification and treatment of patients and prophylactic therapy for uninfected household members
150
Q

What is the bacteria for Tattoo-associated Mycobacterial Infections?

A
  • Mycobacterium chelonae
151
Q

Explain the transmission and manifestations for Mycobacterium chelonae

A
  • emerging agent in tattoo-associated infections
  • skin lesions, papules, pustules, plaques
152
Q

How is tattoo associated mycobacterial infections diagnosed and treated?

A
  • culture, bacterial staining
  • long-term antibiotic treatment, steroids
153
Q

What is Peptic Ulcer disease and gastritis caused by?

A

Helicobacter pylori (H. pylori)

Gram negative

154
Q

Explain what the Peptic Ulcer disease and gastritis bacterium does

A

H. pylori (gram negative) = Class 1 carcinogen!!!!

  • Colonizes gastric mucus-secreting cells (common for ulcer disese)
  • Produces urease, which acts to increase pH
  • Releases toxins that damage epithelial mucosal cells
155
Q

How does H. pylori Disease (Peptic Ulcer disease and gastritis) colonize?

A

Colonizes gastric mucus-secreting cells, beneath gastric mucosa by aid of suface fimbriae (adhesions)

  • Binds sialic acid in gastric epithelial cells

Produces ureases which hydrolyses ammonia and provides a local alkaline environment

Proteases, phospholiases, cytokines, and cytotoxins increase inflammation

156
Q

How is H. pylori Disease (Peptic Ulcer disease and gastritis) transmitted?

A

Probably person to person

common source has not been ruled out

157
Q

How is H. pylori Disease (Peptic Ulcer disease and gastritis) diagnosed?

A

Culture of gastric biopsy specimens, examination of stained biopsies, serological testing, urea breath test, tests for ammonia in urine, and detection of urease activity in biopsies

158
Q

How is H. pylori disease (Peptic Ulcer disease and gastritis) treated, prevented and controlled?

A

a combination of drugs to decrease stomach acid and antibiotics to kill the bacteria

159
Q

What is the organims for Chlamydia STD?

A

chlamydia trachomatis

Gram negative small rods

MOST FREQUENT REPORTED STD

160
Q

What is the bacterial microorganism for gonorrhea STD?

A

Neisseria gonorrhoea

Gram negative diplococci

can affect the mucous membranes of the genitourinary track, eye, rectum and throat

161
Q

What is the bacterial microorganism for syphillis STD?

A

Treponema pallidum

Spirochete-gram stain not used due to difficulty. Prefer dark-field of lesions exudate. Serology-VDRL or RPR testing

A contagious, ulcerative disease

162
Q

What are the clinical manifestations for Chlamydia disease?

A

In males

  • asymptomatic or urethral discharge, and itching and inflammation of genital tract

In femails

  • sometimes asymptomatic
  • may cause PID
  • if pregnant, can lead to miscarriage, stillbirth, inclusion conjunctivitis, and infant pneumonia
163
Q

How is Chlamydia disease diagnosed?

A

demonstration of leukocyte exudate, exclusion of urethral gonorrhea by gram stain and culture, rapid diagnostic tests

164
Q

How is chlamydial diseases treated?

A

antibiotic therapy

165
Q

What causes Gonorrhea? and how does the bacterial attach?

A

Neisseria gonorrhoeae

gram negative, oxidase-positive diplococcus

(referred to as gonococcus)

Attaches to microvilli; phagocytosed by mucosal cells

166
Q

What is the conjunctivitis of the newboar called? Mother to child during birth…

A

ophthalmia neonatorum

167
Q

What are the virulence factors for Gonorrhea?

A
  • Attach to microvilli or mucosal cells by pili and proein II adhesions
  • survive phagocytosis by neutrophils
  • fibrosis results and may lead to stricture or urethral closing
168
Q

What are the clinical manifestations of Gonorrhea?

A

symptoms in men

  • Urethral discharge of yellow, creamy pus, and painful, burning urination

Symptoms in femails

  • vaginal discharge beginning 7 to 21 days after infection
169
Q

What results from the infection of the fallopian tube and surrounding tissue from Gonorrhea?

A

Pelvic inflammatory disease (PID)

  • major cause of sterility and ectopic pregnancies
170
Q

What is the disseminated gonococcal infections?

A

involvement of joints, heart and throat

171
Q

What is teh diagnosis for gonorrhea?

A

culture of bacterium followed by gram stain, oxidase test and determination of cell and colony morphology; DNA probe test

172
Q

What is the treatment, prevention and control for Gonorrhea?

A

Antibiotic therapy (penicillin resistance common)

Public education, diagnosis and treatment of asymptomatic infividuals, condom use, and quick diagnosis and treatment of infected individuals

173
Q

What is the cause of syphilis?

A

Treponema pallidum subsp.pallidum

174
Q

What are the types of syphilis?

A

venereal syphilis - sexually transmitted

congenital syphilis - aquired in utero (from mom)

175
Q

What is the diagnosis for syphilis?

A

clinical history, microscopic examination and serology

176
Q

What is the treatment, prevention and control for syphilis

A

antibiotic therapy most effective in early stages

public education, prompt treatment of new cases, follow-up on sources and contacts, sexual hygiene and use of condoms

177
Q

What are the stages of syphilis

A

Primary/shanker - lesions on genital area

Secondary - lesions all over body

Thertiary stage - 2 to 3 years but up to 10 years after exposure (can lead to demensia and mind loss)

During military take over, syphilis took over and become very common

178
Q

What is staphylococcal disease caused by?

A

members of the genus Staphylococcus

Gram positive cocci

occurring singly, pairs, tetrads or grape-like clusters

179
Q

How would you describe the genus staphylococcus and where does it normally inhabit?

A

facultative anaerobes and usually catalase positive

normally inhabitants of upper respiratory tract, skin, intestines and vagina

180
Q

What are the two main type sof staphylococcal diseases?

A

S. aureus - coagulase positive, pathogenic

S. epidermidis - coagulase negative, less pathogenic but nosocomial opportunists (common on skin and does not cause too much problems, if right place at right time it can become pathogen)

181
Q

What contributes to pathogenicity of staphylococcal diseases?

A

Teichoic acid and peptidoglycan

182
Q

What is staphylococcal diseases harbored by?

A

asymptomatic carriers or active carriers (have the disease)

  • spread by hands, inanimate objects or expelled by respiratory tract, or through blood

**May produce disease in almost every organ and tissue**

  • Immune comprimised most at risk!
183
Q

What are the virulence factors for staphylococcal diseases?

A
  • Exotoxins and enzymes involved in invasiveness
  • toxin genes may reside on plasmids and on chromosome

Examples:

  • enterotoxin - food intoxication
  • bacteremia and abscess formation
184
Q

what is an exotoxin?

A

organism produces a toxin that travels to other areas of the body

185
Q

what is beta lactamase physiological action?

Produced by staphylococci

A

breaks down beta-lactam antibiotics

186
Q

What is catalase physiological action?

Produced by staphylococci

A

converts hydrogen peroxide into water and oxygen and reduces killing by phagocytosis

187
Q

What is coagulase physiological action?

Produced by staphylococci

A

Reacts with prothrombin to form a complex that can cleave fibrinogen and cause the formation of a fibrin clot; fibrin may also be depositited on the surface of staphylococci, which may protect them form destruction by phagocytic cells; coagulase production is synonymous with invasive pathogenic potential

188
Q

What is DNase physiological action?

Produced by staphylococci

A

Destroys DNA

189
Q

What is enterotoxins physiological action?

Produced by staphylococci

A

Are divided into heat-stable toxins of six known types (A, B, C1, C2, D, E); resonsible for the gastrointerestinal upset typical of food poisoning

190
Q

What are exfoliative toxins A and B (superantigens) physiological action?

Produced by staphylococci

A

Cause loss of the surface layers of the skin in scalded-skin syndrome

191
Q

What is Hemolysins physiological action?

Produced by staphylococci

A

Alpha hemolysin destroys erythrocytes and causes skin destruction. Beta hemolysin destroys erythrocytes and sphingomyelin around nerves

192
Q

What is hyaluronidase physiological action?

Produced by staphylococci

A

Also known as spreading factor; breaks down hyaluronic acid located between cells, allowing for penetration and spread of bacteria

193
Q

What is panto-valentine leukocidin physiological action?

Produced by staphylococci

A

Inhibits phagocytosis by granulocytes and can destroy these cells by forming pores in their phagosomal membranes

194
Q

What is lipases physiological action?

Produced by staphylococci

A

breaks down lipids

195
Q

What is nuclease physiological action?

Produced by staphylococci

A

Breaks down nucleic acids

196
Q

What is protein A physiological action?

Produced by staphylococci

A

Is antiphagocytic by competing with neutrophils for the Fc portion of specific opsonins

197
Q

What is proteases physiological action?

Produced by staphylococci

A

Break down proteins

198
Q

What is toxic shock syndrome toxin-1 (a superantigen) physiological action?

Produced by staphylococci

A

Is associated with the fever, shock and multisystem involvement of toxic shock syndrome

199
Q

Explain staphlococcal lesions (localized abscess)

A
  • S. aureus infects a hair follicle, tissue necrosis results
  • coagulase is produced forming a fibrin wall around leasion, limiting spread
  • Liquefaction of necrotic tissue in center of leasion occurs; abscess spreads
  • may be a furuncle (boil) or carbuncle (coalescing of multiple furuncles)
  • Bacteria may spread from area via lymphatics or bloodstream (bacterimia)
200
Q

Explain Staphylcoccal Scalded Skin Syndrome (SSSS)

A
  • caused by strains of S. aureus that carry a plasmid-borne gene for exfoliative toxin (exfoliation)
  • Epidermis peals off revealing red area underneath
  • Staph gets right under the epidermis of skin and starts producing toxins
201
Q

What is the diagnosis for Staphylcoccal Scalded Skin Syndrome (SSSS)?

A

isolation/identification of Staphylococcus involves commercial kits

202
Q

What is the treatment, prevention and control for Staphylcoccal Scalded Skin Syndrome (SSSS)?

A
  • Isolation and identification based on catalase test, coagulase test, serology, DNA fingerprinting and phage typing
  • Antibiotic therapy
    • many drug-resistant strains
  • Personal hygiene, food handling, and aseptic management of lesions
203
Q

Explain staphylococcal disease toxic shock syndrome (TSS)

A
  • caused by S. aureus strains that release toxic shock syndrom toxin and other toxins
  • Some cases occur in femails who use superabsorbant tampons
  • disease results from body’s response to staphylococcal superantigens (T cells fight own body)
  • Tell body T cells we have a problem and kick into overdrive
204
Q

What are the clinical manifestations for staphylococcal disease toxic shock syndrome (TSS)?

A

Low blood pressure, fever, diarrhea, extensive skin rash, and shedding of skin

205
Q

Explain Streptococcal disease superficial types of diseases

A
  • Contact superficial cutaneous diseases:
    • Cellulitis
      • Diffuse, spreading infection of subcutaneous tissue
      • redness and swelling
    • Impetigo
      • Also caused by S. aureus
      • Superficial cutaneous infection commonly seen in children
      • crusty lesions and vesticules surrounded by red border
    • Erysipelas
      • acute infection of dermal layer of skin
      • red patches that may occur periodically at same site for years
206
Q

Explain the Streptococcal Invasive diseases

A

May reach underlying muscles

  • caused by certain virulent strains of S. pyogenes
  • Rapidly progressive
    • carry genes for exotoxins
      • superantigens (select agent)
  • Tissue-destroying protease
  • Clinical manifestations
    • Necrotizing fasciltis (“flesh eating”): destruction of sheath covering skeletal muscles
    • Myositis: inflamation and destruction of skeletal muscles and fat tissue
    • toxic shock-like syndrom (TSLS): precipitous drop of blood pressure, failure of multiple organs and high fever
207
Q

Explain Tetanus and what it is caused by?

A

Caused by Clostridium tetani

  • anaerobic, Gram Positive Spore former
    • Endospores found in soil, dust, hospital environments, and mammalian feces (rusty metal)
  • Produces tetanospasmin in low oxygen tension environments
    • causes prolonged muscle spasms
  • Also produces tetanolysin, a hemolysin
208
Q

What is the method for getting Tetanus?

A

Portal of entry - skin wounds

209
Q

How is Tetanus diagnosed?

A

clinical history of wound infection and muscle stiffness

210
Q

What is the treatment, prevention and control for Tetanus?

A

antibiotic therapy and treatment with antitoxin

active immunization with toxoid (DPT vaccine) and proper care of wounds contaminated with soil, prophylocatic use of antitoxin

211
Q

What are the clinical manifestations of Tetanus?

A

Early in disease

  • Tension or cramping and twisting of skeletal muscles and tightness of jaw muscle

Advanced disease

  • trismus (“lockjaw”), characteristic facial expressions, board-like rigidity of trunk, tonic convulsions, and backward bowing of back
  • Death usually results form spasms of diaphragm and intercostal respiratory muscles
212
Q

What is pink eye?

A

conjuctivitis

  • defined as inflammation of the bulbar and/or papebral conjuctiva (the transparent lubricating mucous membrane that covers both surfaces of the eye).
  • has many etiologies, including infection from various bacteria, fungi, and viruses, as well as toxic and allergic insults
  • Common about 1% of all primary care office visits in US are related to conjuctivitis
  • 30% have bacterial conjunctivitis, though 80% are treated with antibiotics
  • Most common bacteria:

Staphylococcus, streptococcus, corynebacterium, Haemophilus, Pseudomonas, and Moraxella species

213
Q

What are the common bacteria that cause conjunctivitis?

A

Pink eye

  • Most common bacteria:

Staphylococcus, streptococcus, corynebacterium, Haemophilus, Pseudomonas, and Moraxella species

214
Q

What is an inflammation of stomach and intestinal lining?

A

Gastroenteritis

215
Q

What is it when a food is a source of pathogen?

A

food poisoning

216
Q

What is it in food-borne infections that make it different?

A

pathogen must colonize host

217
Q

What is food intoxication?

A

Ingestion of toxin - through bacteria may have died, the toxins they produced make you sick

  • enterotoxins - disrupt functioning of intestinal mucosa causing nausea, vomiting, and/or diarrhea
218
Q

What is the general way to prevent food borne and water borne diseases?

A

sanitation measures

219
Q

What is the reservoir for the organism Aeromonas hydrophilia?

Waterborne Bacterial Pathogen

A

Free-living

sometimes associated with gastroenteritis, cellulitis and other diseases

220
Q

What reservoir does the organism Campulobacter jejuni?

Waterborne Bacterial Pathogen

A

Bird and animal reservoirs

Major cause of diarrhea; common in processed poultry; a microaerophile

221
Q

What reservoir is for Helicobacter pylori?

Waterborne Bacterial Pathogen

A

Free-Living

Can cause gastrititis, peptic ulceers, gastric aderocarcinomas

222
Q

What is the reservoir for Legionella pneumophilia?

Waterborne Bacterial Pathogen

A

Free-living and associated with protozoa

Found in cooling towers, evaporates, condenses, showers, and other water sources

223
Q

What reservoir for Leptospira spp.?

Waterborne Bacterial Pathogen

A

Infected animals

Hemorrhagic effects, jaundice

224
Q

What is the reservoir for Mycobacterium spp.

Waterborne Bacterial Pathogen

A

Infected animals and free-living

COmplex recovery procedure required

225
Q

What is the reservoir for Pseudomonas aeruginosa?

Waterborne Bacterial Pathogen

A

Free-living

Swimmer’s ear and related infections

226
Q

What is the reservoir for Salmonella enteriditis?

Waterborne Bacterial Pathogen

A

Animal intestinal tracts

COmmon in many waters

227
Q

What is teh reservoir for Vibrio cholerae?

Waterborne Bacterial Pathogen

A

Free-living

FOund in many waters, including estuaries

228
Q

What is the reservoir for vibrio parahaemoyticus?

Waterborne Bacterial Pathogen

A

Free-living in coastal waters

causes diarrhea in shellfish consumers

229
Q

What is the reservoir for Yersinia enterocolitica?

Waterborne Bacterial Pathogen

A

Frequent in animals and in the envirionment

Waterborne gastroenteritis

230
Q

What is the bacteria responsible for Botulism?

A

Clostridium botulinum

and obligate anaerobic, endospore-forming

Gram positive rod (on select agent list)

231
Q

Explain the presence of Botulism

A

Most common source of infection is insufficiently heated home-canned foods

  • Endospores not killed, then germinate and produce toxin
  • if food inadequately cooked, toxin remains and causes disease
232
Q

What does Botulism impact?

A

Botulinum toxin

neurotoxin that binds to synapses of motor neurons

233
Q

What is the diagnosis for Botulism?

A

Diagnosis restricted to reference laboratoris

  • Demonstration of toxin in patient’s serum, stool, or vomitus or C. botulinum in stool cultures
234
Q

Explain Botulism in Infants

A

Most common form

  • Endospores ingested, germinate, reporduce and produce exotoxin
  • constipation, listlessness, general weakness, and poor appetite; death may reslut from respiratory failure
235
Q

What is the treatment, prevention and control for Infant botulism?

A
  • symptomatic/supportive therapy and administration of antitoxin
  • safe food processing practices and not feeding honey to babies under one year of age
236
Q

What is the bacteria responsible for Gastroenteritis?

A

Campylobacter jejuni

gram negative

curved rod found in intestinal tract of animals (e.g. chickens, turkey, and cattle)

causes campylobacteriosis

237
Q

How is Gastroenteritis transmitted?

A

to humans by contaminated food or water, contact with infected animals or anal-oral sexual activity

238
Q

What is the manifestation of Gastroenteritis?

A

C. jejuni invades epithelium of small intestine, secretes and exotoxin, causes inflammation, ulceration and bloody stool

239
Q

How is Gastroenteritis diagnosed?

A

culture in low oxygen, high CO2 atmosphere

240
Q

What is the treatment, prevention and control of Gastroenteritis?

A
  • Symptomatic/supportive therapy and antibiotic therapy in severe cases
  • good personal hygiene, safe food handling practices
241
Q

What is the comma-shaped bacteria?

A

Vibrio cholerae (cholera)

Gram - negative bacteria

242
Q

How is Cholera aquired?

A

ingesting food or water contaminated by fecal matter from patient or carrier

243
Q

What is a natural reservoir for V. cholerae (cholera)?

A

shellfish are natural reservoirs

244
Q

How does cholerae adhere to organisms?

A

adhere to intestinal mucosa of small intetine and secrete the toxin choleragen

245
Q

What happens in the presence of the choleragen toxin?

A

Results in a massive loss of water and electrolytes

  • Production of “rice-water stools”
246
Q

How is cholerae diagnosed?

A

culture form feces with subsequent identification by agglutination reactions

247
Q

What is the treatment, control and prevention for cholerae?

A
  • oral rehydration
  • antibiotic therapy
248
Q

What is another name for Escherichia coli - Gastroenteritis?

A

Traveler’s diarrhea

249
Q

What is E. coli - Gastroenteritis (Traveler’s diarrhea) caused by?

A
  • Caused by certain viruses, bacteria or protozoa normally absent from traveler’s environment
  • E. coli is one of major causative agents
    • Six categories or strains are recognized
    • most other E. coli is non-pathogenic
250
Q

What are the pathogenic E. coli strains (name and special feature)?

A
  • Enterotoxigenic E. coli (ETEC)
    • heat stability - produces one or both enterotoxins repsonsible for diarrhea
  • Enteroinvasive E. coli (EIEC)
    • multiplies within intestinal epithelial cells and may produce a cytotoxin and an enterotoxin
  • Enteropathogenic E. coli (EPEC)
    • Causes effacing lesions - destruction of brush boarder microvilli in intestinal epithelial cells
  • Enterohemorrhagic E. coli (EHEC)
    • produces effacing lesions and hemorrhagic colitis, releases shiga-like toxins
  • Enteroaggregative E. coli (EAEC)
    • Forms “stacked brick” appearance of epithelial cells, toxins not been identified
  • Diffusely adhering E. coli (DAEC)
    • Adheres in a uniform pattern to epithelial cells, particular problem in immunologically naive or malneurished children
251
Q

What is the diagnosis for Traveler’s Disease?

A

Past travel history and symptoms, isolation and identification of causative agents using DNA probes, tests for virulence factors and PCR

252
Q

What is the treatment, prevention and control of Traveler’s Disease?

A
  • Symptomatic/supportive therapy and antibiotic therapy
  • Avoiding contaminated food and water
253
Q

What is the cause/bacteria for Salmonellosis?

A

caused by >2,000 Salmonella serovars

Gram negative

Non-spore forming rods

254
Q

How is Salmonellosis transmitted?

A

to humans by contaminated foods such as beef products, poultry, egg products and water

255
Q

What does the Salmonellosis disease impact and what are the symptoms?

A

Disease results from food-borne infection

  • bacteria in intestinal mucosa produce enterotoxin and cytotoxin

Symptoms include abdominal pain, cramps, diarrhea, nausea, vomiting and fever

256
Q

How is Salmonellosis diagnosed?

A

isolation of organism from food or patients’ stool

257
Q

How is Salmonellosis treated?

A

Fluid and electrolyte replacement

good food handling practices, proper refrigeration, adequate cooking

258
Q

What bacteria is responsible for Typhoid Fever?

A

Salmonella enterica

subspecies enterica serovar Typhi

Gram negative rod

259
Q

How is Typhoid Fever aquired?

A

by ingestion of food or water contaminated by feces in infected humans or person to person contact

260
Q

What is another version of Typhoid Fever

A

Paratyphoid fever

  • Milder form of disease
261
Q

How does the Typhoid Fever bacteria spread?

A

From small intestine to lymphoid tissue, blood, liver and gallbladder

262
Q

What are the symptoms of Typhoid Fever?

A

Fever, headache, abdominal pain, anorexia, and malaise

263
Q

What happens in Typhoid Fever carriers?

A

In carriers (eg. Typhoid Mary) bacteria grow in gallbladder and reach intestine through bile duct

264
Q

how does one diagnose Typhoid Fever?

A

demonstration of typhoid bacilli in blood, urine, or stools

serology (Widal test)

265
Q

How does one Treatment, prevention and control of Typhoid Fever?

A
  • Antibiotic therapy
  • vaccine for high risk individuals
  • purification of drinking water, prevention of food handling by carriers, and isolation of patients
266
Q

What bacteria causes shigellosis?

A

Bacillary dysentery

  • caused by four species of genus Shigella
  • Gram negative, non-spore forming rods
  • intracellular parasites, multiply in colonic epithelium
267
Q

What does shigellosis cause?

A

inflammatory reaction in mucosa

humans are the only host

watery stools often contain blood, mucus and pus

268
Q

How is shigellosis diagnosed?

A

biochemical characteristics

serology

269
Q

How is shigellosis treated, prevented and controlled?

A

antibiotic therapy

prevention by use of good personal hygiene and a clean water supply

270
Q

What is the virulence in shigellosis?

A
  • endotoxin
  • Exotoxins play role in disease progression
    • Shiga toxin
    • targets glomerular epithelium and may lead to kidney failure
  • Type III secretion system delivers virulence factors into epithelial cells
271
Q

What does Staphylococcal food poisoning result from?

A

Ingestion of improperly stored or cooked food (eg. ham, processed meats, chicken salad, ice cream and hollandaise sauce) in which staphylococcus aureus has grown and released enterotoxin

272
Q

What does staphylococcal food poisoning produce?

A
  • Bacteria produce heat-stable enterotoxins in food
    • properly cooking the food will not destroy toxin; intoxications can result from thoroughly cooked food
273
Q

What are the symptoms of Staphylococcal Food Poisoning?

A

Include abdominal pain, cramps, diarrhea, vomiting and nausea

274
Q

How is Staphylococcal Food Poisoning diagnosed?

A
  • Based on symptoms or laboratory identification of bacteria from food
  • enterotoxins can be detected in foods by animal toxicity tests
275
Q

What is the treatment, prevention and control for Staphylococcal Food Poisoning?

A
  • Fluid and electrolyte replacement
  • avoidance of food contamination, and control of personnel involved in food preparation and distribution
276
Q

What is Zoonotic Diseases?

A
  • Diseases transmitted from animals to humans
  • A number of important human pathogens begin as normal flora or parasites of animals and then adapt to cause disease in humans
277
Q

What is Anthrax caused by?

A

Bacillus anthracis (select agent)

Gram positive, aerobic endospore forming

Endospores viable in soil and animal products for decades

plasmid encodes genes for anthrax toxin

278
Q

How is Anthrax transmitted?

A

By direct contact with infected animals or their products

portal of entry determines form of disease

BIOTERRORISM AGENT

279
Q

What is the virulence of Anthrax?

A

B. anthracis envades immune system by

  • Capsule which inhibits phagocytosis
  • synthesis of coomplex exotoxin
    • protective antigen - forms hole for entry of other toxins
    • edema factor - fluid release and edema
    • lethal factor - inhibits cytokine production
  • Macrophages die, release toxic contents leading to septic shock, death
280
Q

What are the forms of Anthrax disease?

A
  • Cutaneous (most common)
    • Infection through cut or abrasion of skin
    • Manifestiations: 1-15 day incubation
      • skin papule that ulcerates, headache, fever and nausea
    • Antibiotic therapy effective if caught early
  • Pulmonary anthrax
    • Woolsorter’s disease (sheared lambs - direct animal contact)
    • inhalation of endospores
    • Resembles influenze
    • if bacteria reach the bloodstream, usually fatal
  • gastrointestinal anthrax
    • ingestion of endospores
281
Q

How is Anthrax diagnosed?

A
  • Presumptive ID in sentinel labs of laboratory response network (LRN)
    • Gram-stained smear of skin lesion, cerebrospinal fluid or blood; also growth and biochemical characteristics of culture
  • confirmatory diagnosis by PCR and serology
282
Q

How is Anthrax Treatment, prevented and controlled?

A
  • Antibiotic therapy and symptomatic/supportive therapy
  • Immunization of animals and persons at high risk
283
Q

What is Brucellosis (Undulant Fever) caused by?

A

Brucella spcies (B. abortus, B. melitensis, B. ovis, B. suis, or B. canis) (select agents)

  • Elk to cattle hurds can infect humans
  • Brucella spp. are tiny Gram-negative coccobacilli
284
Q

How are humans infected with Brucellosis?

A
  • Ingestion of Brucella contaminated food or water
  • inhalation of organism
  • bacterial entry into body through skin wounds
285
Q

What are the symptoms of Brucellosis?

A
  • Presents as non-specific, flu-like symptoms
  • In undulant form, symptoms include undulant fevers, arthritis and testicular inflammation in males
  • In chronic form, symptoms include chronic fatigue syndrome, depression and arthritis
286
Q

What causes Psittacosis (ornithosis)?

A

Chlamydophilia psittaci

enters respiratory tract, transported to and reproduces in liver and spleen and then invades lungs

287
Q

Explain the details of Psittacosis (Ornithosis), how is it transmitted?

A

Infectious disease of birds

  • Transmitted to humans by direct contact with infected birds or by inhalation of dried bird excreta
  • occupational hazard in poultry industry
288
Q

What are the clinical manifestations of Psittacosis (ornithosis)?

A

Inflammation and hemorrhaging of lung tissue and pneumonia

289
Q

How is Psittacosis (ornithosis) diagnosed?

A

Isolation from blood or sputum, or by serology

290
Q

How is Psittacosis (ornithosis) treated, prevented and controlled?

A

antibiotic therapy

chemoprophylaxis for pet birds and poultry

291
Q

What causes Q fever (Select Agent)?

A

Coxiella burnetii

intracellular Gram- Negative bacterium

proliferates in lungs

servives outside host by forming endospore-like body

Q = quiry because do not know what is going on

292
Q

How is Q fever transmitted?

A
  • Ticks between animals
  • Contaminated dust to humans
  • Occupational hazard among slaughterhouse workers, farmers and veterinarians
293
Q

What are the clinical manifestations of Q Fever?

A
  • Mild respiratory symptoms and acute onset of severe headache, muscle pain, and fever
  • endocarditis can develop 5 to 10 years later
294
Q

How is A Fever Diagnosed?

A

In reference labs using immunofluorescence

295
Q

What is the treatment, prevention and control of Q fever?

A
  • Serological tests
  • antibiotic therapy
  • vaccination of high risk individuals and pasturization of cow and sheep milk in areas where disease is endemic
296
Q

What is Tularemia caused by?

A

Francisella tularensis (Select Agent - Category A)

297
Q

How is Tularemia spread?

A

From animal reservoirs by serveral mechanisms (from rabbits)

  • Arthropod bites
  • direct contact with infected tissue
  • inhalation of aerosolized bacteria
  • ingested of contaminated water or food
298
Q

What are the clinical manifestations of Tularemia?

A

incubation 2 to 10 days

primary ulcerative lesion at infective site, enlarged lymph nodes and high fever

299
Q

How is Tularemia diagnosed?

A

PCR, culture of bacteria and immunodiagnostic tests

300
Q

How is Tularemia treated, prevented and controlled?

A
  • antibiotic therapy

public education, protective clothing, vector control and immunization for high- risk individuals

301
Q

What are opportunistic diseases?

A

Microbes that are otherwise members of the normal microbiota but become pathogens are referred to as opportunists and cause opportunistic disease

302
Q

What is the bacteria for Antibiotic - Associated Colitis (pseudomembranous Colitis)?

A

Clostridium difficile (C. difficile associated diarrhea - CDAD)

  • uncomplicated diarrhea
  • pseudomembranous colitis
    • viscous collection of inflammatory cells, dead cells, necrotic tissue, and fibrin that obstructs the intestine
  • toxic megacolon
    • inflammation resulting in intestinal tissue
303
Q

What is C. difficile?

A

Anaerobic spore forming bacillus found in the intestines of some healthy people

  • Numbers in check by other normal intestinal microbiota
  • excessive antibiotic use eliminates normal microbiota and allows C. difficile to overgrow
    • most common: amoxicillin, ampicillin, clindamycin, cephalosporins
304
Q

What are the virulence factors of C. difficile?

A

Multiplies and produces toxins

Toxin A (enterotoxin causing diarrhea)

Toxin B (cytotoxin kills cells)

305
Q

what are the clinical manifestations and treatment for C. difficile?

A

Inflammation, diarrhea, fever, nausea, cramping

most common cause of diarrhea in hospitalized patients

treatment is with antibiotics

306
Q

What is Bacterial vaginosis caused by?

A
  • Gardnerella vaginalis
    • Gram positive or gram variable pleomorphic nonmotile rods
  • Mobiluncus spp
    • Gram-negative anaerobic rod
307
Q

Explain the Bacterial vaginosis disease, details and transmission

A

Typically a mild disease, characterized by

  • copious, frothy, fishy-smelling vagina discharge
  • varying degrees of pain/itching

Microbes are present in vagina and rectum of 20-40% of healthy women, suggesting an opportiunistic etiology

  • transmission from person to person through intimate contact can occur, however
308
Q

How is Bacterial vaginosis diagnosed and treated?

A
  • Diagnosis via microscopic observation of clue cells - vaginal epithelial cells covered in bacteria
  • Treatment with metronidazole clears the infection
309
Q

How are Dental diseases acquired?

A

Acquired enamel pellicle

  • formed when enamel absorbs acidic glycoproteins from saliva
  • colonized by various bacterial species to form plaque

Coaggregation

  • attachment of different species of bacteria to each other
  • based on cell-to-cell recognition
310
Q

What is the main species involved in periodontal disease?

A

Porphyromonas gingivalis

311
Q
A

BIOM 360 (7 decks)

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