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Micro > Exam 4 > Flashcards

Exam 4 Flashcards

1
Q

what are some LRT infections

A
  • bronchitis
  • histoplasmosis
  • influenza*
  • pneumonia
  • tuberculosis
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2
Q

what are some URT infections

A
  • common cold
  • diphtheria
  • whooping cough
  • strep throat
  • ear infections
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3
Q

how are respiratory pathogens transmitted from human to human

A
  • via indirect contact with respiratory droplets (common)
    • less than 3ft; are heavier and need to be in
      close contact with someone to transfer
  • via airborne droplet nuclei (rare)
    • are lighter and can travel in the air for a
      longer amount of time
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4
Q

true or false; some respiratory pathogens exist as part of the normal microbiota

A

true

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5
Q

does influenza start in the URT or LRT

A

starts in the URT and then moves to LRT

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6
Q

describe corynebacterium diphtheriae shape

A
  • gram-positive rods
  • often arranged side by side in “palisades”
  • irregular staining
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7
Q

how is corynebacterium diphtheriae transmitted

A
  • humans are the only known reservoir
  • transmitted via contact with respiratory droplets
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8
Q

humans can have c. diphtheriae in their

A

oropharynx or on skin

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9
Q

what population is most likely to get c. diphtheriae

A

unimmunized children

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10
Q

describe diptherotoxin

A
  • A-B exotoxin
  • lysogenzied strains of C. diphtheriae causes Diphtheria
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11
Q

what is the function of diptherotoxin

A

inhibits protein synthesis

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12
Q

what are some signs/symptoms of diphtheria

A
  • acute onset of sore throat
  • pseudomembrane = dead cells, exudate, RBCs, and bacteria
  • “bull neck” = enlarged cervical lymph nodes and edema in the neck
  • fever
  • systemic diphtheria = toxin gets into circulation (toxemia) and damages heart and kidneys
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13
Q

if someone were to have a sore throat, enlarged cervical lymph nodes, fever, and pseudomembrane - what would be their diagnosis?

A

diphtheria

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14
Q

would corynebacteria organisms be detected in the blood from a patient with systemic diphtheria?

A

no
- because the corynebacteria infect the URT, but the localized infection produces the toxin that would be systemic

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15
Q

c. diphtheria requires these two treatments

A
  1. antibiotics to arrest the infection, but toxins already absorbed are unaffected
  2. diphtheria antitoxin to neutralize toxin circulation
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16
Q

what vaccines work to prevent diphtheria, pertussis, and tetanus

A

DTaP and Tdap vaccines
- contains diphtheria toxoid = inactivated exotoxin

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17
Q

what are some signs/symptoms of a common cold and how long do they last

A
  • sneezing, sore throat, runny nose, cough
    • nasal secretions initially watery, then thicken,
      finally become cloudy and greenish
  • symptoms mostly gone within 7-10 days
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18
Q

what are some complications that can occur with a common cold

A

sinus congestion or earache

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19
Q

what are some signs/symptoms of the flu and how long do they last

A
  • high fever; lasts 3-4 days
  • early and prominent extreme exhaustion
  • chest pain and severe cough
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20
Q

what are some complications that can occur with the flu

A
  • bronchitis and pneumonia; can be life-threatening
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21
Q

how many times do adults vs children get a common cold and what is the causative agent?

A
  • adults get ~ 2-4 a year
  • children get ~ 9 colds a year
  • causative agent = children don’t have as much immunity
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22
Q

what is the most common cause of the common cold

A

rhinovirus

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23
Q

describe rhinovirus

A
  • naked virus with an RNA genome
  • replicate best between 33C - 35C -> infect cooler tissues of the nose
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24
Q

what is the pathogenesis of common cold

A
  • infects respiratory epithelial cells in the nasal mucosa
  • inhibits the ciliary motion of infected cells; cells die
  • damage leads to release of cytokines, inflammation
  • nasal excess nasal secretions, congestions, sore throat, coughing, and sneezing
  • fever is typically absent
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25
Q

how is rhinovirus transmitted

A
  • direct contact = with hands contaminated with respiratory droplets
  • indirect contact = respiratory droplets
  • contaminated fomites (rhinoviruses are naked)
  • only need a few virions to infect
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26
Q

describe bordetella pertussis

A
  • tiny encapsulated gram-negative bacilli
  • causes pertussis aka whooping cough
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27
Q

bordetella pertussis is the classic disease of

A

infants (<1 year)
- severe, life-threatening in babies

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28
Q

what is the epidemiology of bordetella pertussis

A
  • human reservoir
  • transmitted via contact with respiratory droplets
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29
Q

what is the pathogenesis of bordetella pertussis

A
  • cells are inhaled, attach to ciliated cells of respiratory epithelium
  • tracheal cytotoxin = toxic to ciliated epithelial cells -> disrupts mucociliary clearance
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30
Q

describe pertussis toxin (PTx)

A
  • A-B exotoxin
  • A subunit inactivates inhibitory regulatory G protein, causing increase in cAMP production
  • increased cAMP yields increased mucus, decreased killing ability of phagocytes
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31
Q

what are the stages of pertussis disease

A
  1. incubation = 7-10 days; no symptoms; rising bacterial culture
  2. catarrhal = 1-2 weeks; rhinorrhea, malaise, fever, sneezing, anorexia; peak bacterial culture
  3. paroxysmal = 2-4 weeks; repetitive cough with whoops, vomiting, leukocytosis; falling bacterial culture
  4. convalescent = 3-4 weeks (or longer); diminished paroxysmal cough, development of secondary complications (pneumonia, seizures, encephalopathy); lowest point of bacterial culture
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32
Q

what is the treatment for pertussis

A
  • primarily supportive
  • antibiotics effective if treated early
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33
Q

what is the prevention of pertussis

A
  • immunization with DTaP starting at two months
  • subunits of B. pertussis are used in the vaccine
  • requires boosters, Tdap
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34
Q

what does Tdap include

A

tetanus toxoid, reduced diphtheria toxoid, and acellular pertussis

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35
Q

which type of vaccine do you think would result in longer lasting immunity?
- whole cell vaccine
- subunit (acellular) vaccine

A

whole cell vaccine

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36
Q

describe the symptoms of and how long the immunity for killed whole-cell vaccine, DTP

A
  • fever, agitation, febrile seizures
  • long term immunity
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37
Q

what are the symptoms and duration of immunity for acellular vaccines, DTaP

A
  • fewer, milder side effects
  • waning immunity
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38
Q

during which weeks should pregnant women get a dose of Tdap vaccine and why

A
  • during the early part of gestational weeks 27 through 36
  • helps mother from passing pertussis onto infant and provides passive immunity to infant
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39
Q

what is the route of infection of bacterial pneumonia

A
  • the infection of the lungs elicits inflammation
  • the alveoli fill with fluids and WBCs (consolidation)
  • air exchange becomes impaired and patients experiences respiratory distress
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40
Q

describe klebsiella penumonia

A
  • gram-negative rods
  • large capsule is its major virulence factor
  • produces big mucoid colony when cultured on agar
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41
Q

what are some symptoms of klebsiella pneumonia

A

lung necrosis and abscess formation resulting in bloody “currant jelly” sputum

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42
Q

klebsiella pneumonia is the leading cause of

A

hospital-acquired pneumonia

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43
Q

how is klebsiella pneumonia transmitted

A
  • transmitted via contact with respiratory droplets or contaminated medical equipment (eg ventilators)
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44
Q

true or false - klebsiella penumoniae may be part of the microbiota in pharynx and GI tract, and do not typically cause respiratory disease in healthy individuals

A

true

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45
Q

what populations are at most risk for klebsiella pneumonia

A
  • those with preexisting lung conditions
  • patients with invasive medical devices
  • alcoholics and diabetics
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46
Q

what is the treatment for klebsiella pneumonia

A
  • carbapenem antibiotics (beta lactam antibiotic)
  • though it is hard to treat klebsiella pneumonia because of its antibiotic resistance
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47
Q

new strains encoding klebsiella pneumonia have emerged carbapenemase (KPC) and they belong to a family of bacteria called

A

carbapenem-resistant enterobacteriaceae (CRE)

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48
Q

describe mycoplasmal pneumonia

A

small, easily deformed bacteria lacking cell wall (no peptidoglycan)

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49
Q

mycoplasmal pneumonia is the leading pneumonia of

A

college students, common among military recruits, and children 5-15 years of age

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50
Q

how is mycoplasmal penumonia transmitted

A

through contact with respiratory droplets
- not part of the microbiota

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51
Q

mycoplasmal penumonia use specialized attachment organelle to bind to

A

ciliated cells
- this causes epithelial cells to be damaged and ciliary motion is hindered

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52
Q

what are some signs/symptoms of mycoplasmal pneumonia

A
  • generally mild “walking pneumonia” or “atypical pneumonia”
  • onset is gradual
  • initial symptoms are fever, headache, muscle pain, and fatigue
  • dry persistent cough and sputum may be produced later
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53
Q

describe haemophilus influenzae penumonia

A
  • gram-negative coccobacillus
  • nonencapsulated strains, which cause pneumonia
  • colonizes the nasopharynx in majority of healthy children
  • elderly is the high risk group
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54
Q

how is haemophilus influenzae transmitted

A
  • via contact with respiratory droplets
  • infect alveoli -> inflammation -> exudate rich in neutrophils -> cough and shortness of breath
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55
Q

antibiotic resistance is a big challenge for treatment of

A

haemophilus influenzae
- no vaccine against the nonencapsulated strains

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56
Q

describe histoplasmosis (spelunker’s disease)

A
  • dimorphic fungus (ie mold and yeast forms)
  • exists in soil contaminated with bat or bird droppings
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57
Q

how is histoplasma transmitted

A
  • reservoir: birds and bats
  • acquired through inhalation of mold spores from soil (often soil contaminated with bird and bat droppings)
  • airborne transmission = the spores become airborne during cleanup or demolition projects
  • non-communicable
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58
Q

what are some signs/symptoms of histoplasma

A
  • headache, weakness, chest pain, and in severe cases -> extensive pulmonary infiltration and dissemination to other organs
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59
Q

what other diseases may occur from histoplasmosis

A

serious lung disease (TB-like illness) may occur in immunocompromised people or elderly or infants

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60
Q

what does antigenic drift mean

A

when envelope proteins continually mutate
- resulting from RNA replication errors
- RNA polymerase has low fidelity
- gradual
- occurs with influenza A, B, and C

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61
Q

what does antigenic shift mean

A

major changes caused by genetic reassortment
- coinfection with two viruses in same cells allow mixture of 8 RNA segments
- abrupt
- occurs with influenza A only

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62
Q

if someone has a low grade fever, runny nose, sneezing and cough but feels well enough to work or class, which disease do they most likely have?
- strep throat
- a cold
- flu

A

a cold

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63
Q

what are some symptoms of influenza “the flu”

A

fever, headache, muscle aches/pains, fatigue, sore throat and cough

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64
Q

how is influenza transmitted

A
  • contact with respiratory droplets
  • airborne via respiratory droplet nuclei
  • contact with fomites contaminated with respiratory droplets
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65
Q

describe influenza virus

A
  • enveloped
  • (-) ss RNA genome
  • segmented genoma
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66
Q

what is the pathogenesis of “flu”

A
  • the virus attaches to and infects epithelial cells in the URT
  • replicates inside the cells, damaging the cells (recovery of the mucociliary escalator may take weeks)
  • spreads to LRT and sometimes secondary bacterial infections occur
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67
Q

what are influenza’s glycoproteins “spikes”

A
  • hemagglutinin (HA)
  • neuraminidase (NA)
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68
Q

what is the function of hemagglutinin

A
  • facilitates viral entry
  • binds to sialic acid on host cells which act as receptors
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69
Q

what is the function of neuraminidase

A
  • facilitates virion release from the cell by cleaving sialic acid
  • degrades mucin layer of respiratory tract
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70
Q

why does influenza cause annual epidemics and periodic pandemics

A

viral evolution

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71
Q

flu pandemics are caused by the emergence of a virus that is “novel” which means there is a new

A

HA or NA subtype

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72
Q

HA and NA surface antigens change as influenza

A

replicates

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73
Q

which types of genetic change is primarily responsible for pandemics
- antigenic drift
- antigenic shift
- both are equally as likely to contribute to the emergence of a pandemic viral strain

A

antigenic shift

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74
Q

swine is susceptible to which two strains

A

avian and human influenza strain

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75
Q

true or false - influenza A can infect animals other than humans

A

true

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76
Q

in the 1918 pandemic influenza, were people with the strongest or weakest immune systems affected

A

strongest

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77
Q

what helped contain the 1918 flu pandemic

A

non-pharmaceutical interventions (NPI)
- isolation, quarantine

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78
Q

what is another name for avian H5N1 influenza

A

bird flu

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79
Q

is avian H5N1 influenza highly virulent in humans

A

yes

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80
Q

what are the three qualities that made 1918 influenza pandemic so severe

A
  1. everyone was susceptible because it was a novel strain
  2. spreads easily from person-to-person (airborne transmission)
  3. virus was unusually virulent (mortality rate = ~10%)
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81
Q

evidence so far suggests that H7N9 and H5N1 influenza cannot be transmitted from

A

human to human

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82
Q

what is the treatment for influenza antivirals

A
  • supportive treatment (rest and fluids)
  • there are four FDA-approved antiviral drugs recommended by CDC to treat flu
    • three of which are NA inhibitors
    • needs to be given early
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83
Q

what is the prevention of the four influenza strains

A

flu vaccines
- takes about six months to produce a flu vaccine
- vaccines are protective if the vaccine strains are closely related to circulating strains

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84
Q

describe flu vaccines

A
  • contain three or four different viruses (mix of A subtypes and a B strain)
  • about 50-70% effective, new one required each year because of antigenic drift
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85
Q

what are the two types of flu vaccine

A
  • inactivated vaccine (flu shot)
  • live attenuated vaccine (nasal spray)
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86
Q

what are the inactivated influenza vaccine recommendations

A
  • routine annual influenza vaccination is recommended for all persons aged >_ 6 months who do not have contraindications
  • exceptions: egg allergies and pervious adverse reactions to vaccine
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87
Q

infected people who are asymptomatic or mildly symptomatic can transmit influenza virus to

A

persons at high risk for complications from influenza

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88
Q

what is a coronavirus

A
  • large family of enveloped viruses
  • ss RNA genome
  • cause a range of illnesses from mild to severe
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89
Q

which types of diseases are caused by coronaviruses

A
  • common cold
  • SARS (severe acute respiratory syndrome)
  • MERS (middle east respiratory syndrome)
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90
Q

how is coronavirus transmitted

A
  • contact with respiratory droplets (most)
  • airborne transmission via droplet nuclei (less common)
  • fomites: contaminated with respiratory droplets
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91
Q

when are people most infectious with COVID-19

A

2-3 days before symptoms and first 7 days of illness

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92
Q

what populations are more at risk for COVID

A
  • people older than 65
  • people with underlying medical conditions
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93
Q

what is the structure of SARS CoV-2

A
  • ss (+) RNA genome
  • enveloped
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94
Q

why do S-proteins bind to ACE2

A

triggers either viral endocytosis or membrane fusion and viral entry
- contributes to high rate of infectivity

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95
Q

S protein is coated in ____ which disguise it from the immune system

A

glycans

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96
Q

if SARS CoV-2 is not blocked by the immune system what will happen

A

virions will migrate to the LRT where they infect type 2 pneumocyte cells that are rich in ACE2 proteins
- will eventually lead to apoptosis and death of alveolar cells

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97
Q

in critical cases, a “cytokine storm,” an overreaction by the immune system, causes immune cells to cause damage to

A

healthy tissues

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98
Q

SARS CoV-2 once it infects the alveoli of the lung, may cause hypoxemia. What is hypoxemia?
- low hemoglobin in the blood
- loss of surfactant
- low oxygen in the blood
- septic shock
- elevated oxygen in the blood

A

low oxygen in the blood

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99
Q

what are the three stages of COVID-19

A
  1. asymptomatic state
  2. upper airway and conducting airway response
  3. hypoxia, progression to acute respiratory distress syndrome (ARDS) within 8 to 12 days
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4
5
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100
Q

what happens in stage 1 of COVID

A
  • incubation time - average is 5 days, range 2 to 14 days
  • virus shed by the host in droplets
  • virus propagates, mild innate immune response initiated
How well did you know this?
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101
Q

what happens in stage 2 of COVID

A
  • robust immune response
  • clinical manifestations of disease appear on average 5 days post-exposure and include cough, fever, shortness of breath, sore throat, loss of taste and/or smell
  • up to 80% of COVID-19 cases will either be asymptomatic or will arrest at this stage
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102
Q

what happens in stage 3 of COVID

A
  • critical care/hospitalization necessary
  • manifestations include pneumonia, etc
  • oxygen levels fall (SpO2 < 94%) as lungs become filled with fluid, WBCs, mucus, and cellular debris
  • leading cause of death is hypoxic respiratory failure complicated by ARDS
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103
Q

about four weeks after COVID-19 initial infection, symptoms may include

A

fatigue, joint pain, chest pain, anxiety, depression, worsened quality of life

104
Q

multisystem inflammatory syndrome in children (MIS-C) with exposure to SARS-CoV-2 symptoms include

A

persistent fever, hypotension, rashes, multiorgan involvement (kidneys, heart, GI, vasculature, neurologic), and inflammation

105
Q

describe RT-PCR test; what kind of test is it, what does it detect, lists advantages and disadvantages

A
  • molecular test
  • detects viral genetic material
  • adv: accurate is sample is taken approximately 5 days post-exposure
  • disadv: may not catch early infection, takes 24-48 hours for results
106
Q

describe antigen rapid test; what kind of test is it, what does it detect, lists advantages and disadvantages

A
  • immunological test
  • detects viral protein antigens vs genetic material
  • adv: results in ~15 minutes, good screening tool
  • disadv: not as sensitive as PCR test -> can result in false negatives
107
Q

what are the two diagnostic tests for COVID-19

A
  • RT-PCR test
  • antigen rapid test
108
Q

which viral antigen is targeted by the SARS CoV-2 vaccines currently approved for use in the U.S.
- envelope protein
- spike glycoprotein
- nucleocapsid protein
- envelope lipid
- viral RNA

A

spike glycoprotein

109
Q

what is the goal of COVID-19 vaccines

A
  • to induce the production of antibodies that bind to the virus
  • effectively blocking entry into the host cell so that S protein is the antigen used in most vaccine candidates
110
Q

what are the four COVID-19 treatments

A
  • remdesivir - anti-viral
  • paxlovid - anti-viral
  • bebtelovimab - anti-SARS CoV2 monoclonal antibodies
  • dexamethasone - anti-inflammatory
111
Q

describe remdesivir anti-viral treatment

A
  • nucleosides analog that targets the RNA-dependent RNA-polymerase
  • inhibit viral replication by terminating RNA transcription prematurely
  • IV infusion at a healthcare facility for three days
112
Q

describe paxlovid anti-viral treatment

A
  • protease inhibitor of the SARS-CoV2 main protease enzyme
  • used to treat mild-to-moderate COVID-19 and who are at high risk for progression to severe COVID-19
  • taken at home by mouth (orally)
113
Q

describe bebtelovimab anti-SARS CoV2 monoclonal antibodies treatment

A
  • IgG antibody that binds the spike protein on SARS CoV2
  • blocks attachment to human ACE2 receptor
  • single IV injection
  • FDA does not recommend use of convalescent plasma
114
Q

describe dexamethasone anti-inflammatory treatment

A
  • steroid
  • relieves inflammation
  • recommended only in hospitalized and severe cases if remdesivir cannot be obtained
115
Q

mycobacterium tuberculosis is a chronic granulomatous disease of the lungs but can spread to

A

extrapulmonary organs
- especially in children and HIV patients

116
Q

mycobacterium tuberculosis causes tuberculosis and is the leading

A

infectious disease killer in the world

117
Q

which of the following stains could we use to detect mycobacterium tuberculosis
- gram
- spore
- acid-fast

A

acid-fast

118
Q

describe the shape of mycobacteria and its cell wall

A
  • rods
  • gram (+) cell wall but stains very weakly with gram stain
  • complex cell wall rich in lipids called mycolic acids
    • lipids account for 60% of cell wall weight
119
Q

describe acid-fast cell wall

A
  • resistant to detergents, many antibiotics, and drying conditions
  • slow growth
  • protection from lysis after phagocytosis (along with the capsule)
    • blocks fusion of phagosome with lysosome
    • masks PAMPS on the bacterial surface
    • capacity for intracellular growth within
      macrophages -> “facultative intracellular
      pathogen”
120
Q

what is the epidemiology of TB

A
  • humans are the only natural reservoir
  • airborne transmission (ie respiratory droplet nuclei)
  • very contagious (RO=12)
  • low infectious dose (just about 10 bacilli)
121
Q

what populations are at greatest risk for TB disease

A
  • HIV+ individuals
  • diabetics
  • substance abusers
  • low body weight/malnourishment
  • immunocompromised
122
Q

majority of TB cases in the US occur in which kind of patients

A

foreign-born and HIV-infected

123
Q

infection by mycobacterium tuberculosis typically results in

A

asymptomatic lung infection

124
Q

can immune response controls eliminated TB

A

no

125
Q

TB yields

A

latent tuberculosis infection (LTBI)

126
Q

people who have had TB may develop ____ later in life

A

active tuberculosis disease (ATBD)
- weight loss, night sweating, persistent cough, often blood-streaked sputum

127
Q

what is the pathogenesis of tuberculosis

A
  1. acid-fast bacilli are inhaled and spread to alveoli
  2. phagocytized by alveolar macrophages
  3. M. tuberculosis capsule and waxy mycolic acids block phagosome from fusing with lysosome to avoid destruction within macrophages
  4. mycobacteria multiply in macrophages (intracellular pathogen). inflammatory response -> other phagocytes are attracted to the site
  5. macrophages fuse together to form giant multinucleated cells
  6. a granuloma (aka a tubercle) forms
128
Q

what is the pathogenesis of active secondary TB disease (A2TBD)

A
  • suppressed cell mediated immunity -> macrophages in tubercle die -> mycobacteria, enzymes, cytokines released -> forming area of necrosis
129
Q

what happens in A2TBD

A
  • tubercle ruptures, releases live mycobacteria into airways
  • causes large lung defect called tuberculous cavity
130
Q

how can A2TBD be transmitted

A

by coughing

131
Q

what are the signs/symptoms of active pulmonary TB disease

A
  • most TB cases are pulmonary:
    • chronic cough, blood rust-colored sputum, high
      fever, night sweats, weight loss, and fatigue
132
Q

describe extrapulmonary TB

A
  • bacteria that can spread to organs other than the lungs such as lymph nodes, brain, kidneys, bones
  • called “miliary” TB -> when TB gets into circulation and spreads systemically to all parts of the body
133
Q

extrapulmonary TB is most common in

A

children < 5 years and in HIV-infected patients

134
Q

in an HIV-infected person, TB can develop in one of two ways:

A
  1. person with LTBI becomes infected with HIV and then develops TB disease as the immune system is weakened
  2. person with HIV infection becomes infected with M. tuberculosis and then rapidly develops TB disease
135
Q

explain the process of tuberculin (aka mantoux) skin test for exposure to TB

A

purified protein derivatives (PPDs) from the Mtb bacterium are inserted intradermally and read 48-72 hours later

136
Q

describe the lab detection of mycobacteria

A
  • acid-fast bacilli (“AFB”) in sputum
    • a positive test for AFB in sputum means the person has active TB
    • but…slow growth, 4-6 weeks
  • new rapid PCR-based test: 1-5hours
137
Q

what does BCG TB vaccine stand for

A

bacille calmette-guerin TB

138
Q

how to prevent TB with BCG TB vaccine

A
  • vaccine contains a live attenuated BCG strain
  • BCG is a strain of mycobacterium bovis
    • M. bovis causes TB in cows as well as humans
  • most effective in preventing TB disease in babies and children
  • has very limited effectiveness against pulmonary TB in adults
  • not generally recommended in US
  • used where TB is endemic
139
Q

why are mycobacteria difficult to treat

A
  • replicate slowly
  • replicate intracellularly within macrophages
  • cell wall is difficult to penetrate
  • evolution of drug resistance
140
Q

what is the treatment for mycobacteria

A
  • people with LTBI can be given treatment to prevent them from developing TB disease
  • combination antibiotic therapy taken every day for 6 months for uncomplicated TB, otherwise 12-18 months is standard and even longer if MDR-TB strain
  • DOTS = direction observation treatment system
141
Q

why do we still have TB

A
  • treatment and prevention are difficult
    • slow insidious disease
    • long treatment duration
    • BCG vaccine is inexpensive but inadequate
    • LTBI is a silent reservoir
  • affects the poor disproportionately
    • expensive to both individual and society
    • access to care for diagnosis and treatment
    • contact tracing and DOTS
  • HIV
  • emergence of drug-resistant strains
142
Q

like herpes simplex virus, which of the following belongs to the herpesviridae family
- rubeola virus
- rubella virus
- varicella zoster virus
- influenza

A

VZV

143
Q

what are the two serotypes of herpes simplex virus and how are they transmitted

A
  • HSV-1 = primarily oral contact
  • HSV-2 = primarily genital contact
144
Q

what is the epidemiology of HSV

A
  • virus transmitted by direct contact
    • greatest risk is contact with lesions or saliva
      within few days of disease onset since many
      virions present
    • asymptomatic people can still be infectious
    • can also be transmitted vertically by crossing the
      placenta
145
Q

what happens in the establishment of latent infection of HSV

A
  1. virus penetrates into skin, where it replicates - PRIMARY
  2. virus enters cutaneous neurons and migrates to a ganglion, where it remains in a latent state - LATENT
146
Q

what happens in the reactivation of latent virus of HSV

A
  1. virus can be subsequently be reactivated and travel through sensory neurons to the epidermis
  2. a reccurent infection results
147
Q

in what cells do primary acute infections occur

A

epithelial cells

148
Q

latent infection of HSV persists in

A

sensory neurons in the ganglion

149
Q

what can reactivate HSV

A

stresses like menstruation, sunlight, fever, and illness

150
Q

describe the primary acute infection of labial herpes

A
  • cold sores
  • small blisters near mouth that break in a day or two
  • blisters rupture -> painful superficial ulcers
  • lesions heals within about 10 days, but virus persists throughout life as latent virus
151
Q

describe recurrent infection from reactivation of latent virus of labial herpes

A
  • cold sores
  • usually less severe than initial infection
  • includes tingling, itching, burning on lips
  • blisters and ulcerations usually heal within 7-10 days
152
Q

why aren’t antibodies to HSV-1 protective against the recurrence of the disease?
- in general, antibodies can never bind to antigens on viruses and therefore are never protective
- the person is getting infected with a different serotype
- the virus is contained within neurons and the antibodies cannot penetrate the cells

A

the virus is contained within neurons and the antibodies cannot penetrate the cells
- no viral replication, so cannot recognize infection

153
Q

the mumps virus causes which disease

A

mumps

154
Q

are mumps enveloped, what is their reservoir, how is it transmitted, and how contagious is it

A
  • enveloped
  • human reservoir
  • airborne transmission via respiratory droplet nuclei
  • highly contagious
155
Q

what are the signs/symptoms of mumps

A
  • acute parotitis: painful swelling of the parotid salivary glands
  • fever, pain in swallowing, nasal discharge
156
Q

what are some complications of mumps infection

A
  • viremia may occur (viruses present in bloodstream)
  • complications are rare but include:
    • orchitis (inflammation of the testicles) in
      postpubertal males -> in rare cases, infertility
    • encephalitis - inflammation of brain
    • meningitis - inflammation of fluid and
      membranes surrounding brain and spinal cord
    • deafness
157
Q

what is the immunity and prevention of mumps

A
  • there is only one serotype so infection usually confers life-long immunity
  • live, attenuated vaccine (MMR)
158
Q

what is oral thrush caused by

A

overgrowth of the opportunistic yeast, candida albicans, which is part of the oral microbiota

159
Q

what type of infection of oral thrush; exogenous or endogenous

A

endogenous
- non-transmissible

160
Q

what are the risk groups of oral thrush

A
  • most common in infants because they do not yet have well developed immune systems and have not acquired the robust normal microbiota that keeps candida in check in adults
  • common in AIDS patients
161
Q

what are the signs/symptoms of oral thrush

A

thick, white, “cottage-cheese,” adherent growth on the mucous membranes of mouth and throat
- can easily be wiped off to expose an erythematous mucosa

162
Q

what are two viral disease of the upper digestive system (UDS)

A
  • labial herpes caused by herpes simplex virus
  • mumps caused by mumps virus
163
Q

what is a fungal disease of the UDS

A

oral thrush by candida albicans

164
Q

what is a bacterial disease of the UDS

A

peptic ulcers by helicobacter pylori

165
Q

what are signs/symptoms of peptic ulcers

A
  • epigastric pain
  • heart burn
  • nausea associated with eating
166
Q

what causes peptic ulcers

A

in most cases, caused by bacteria

167
Q

what is the shape of helicobacter pylori

A

gram negative curved rods (vibrio) or spiral (spirillum) shaped

168
Q

what does helicobacter pylori cause

A
  • 90% of peptic ulcers
  • gastritis
  • cofactor in stomach cancer
169
Q

what is the reservoir of helicobacter pylori and how is it transmitted

A
  • human reservoir
  • transmitted via by person-to-person saliva or fecal-oral
170
Q

why doesn’t helicobacter pylori get killed by stomach acids

A
  • H. pylori goes to region of stomach (pyloric region) where the pH of the stomach is relatively higher
    • it can sense pH and actively swim via flagella to
      the region that has a higher pH
  • H. pylori produces urease which breaks urea down into ammonia, this further increases the pH of the stomach
171
Q

what is the pathogenesis of peptic ulcers

A
  • bacteria penetrate and multiply in mucus layer
  • bacteria attach but do not invade epithelium
  • bacterial toxins and the inflammatory response damages mucus-secreting cells
  • acid juices damage to the exposed tissue, causing a peptic ulcer
172
Q

how does someone diagnose H. pylori

A
  • endoscopy to visualize the GI tract and to take biopsy specimen
  • a gastric mucosal biopsy and urease test
    • biopsy sample is placed in media containing urea
    • if H. pylori is present, its urease will hydrolyze the
      urea, causing a pH shift and color change
      • negative urease test = yellow/orange
      • positive urease test = pink
173
Q

what is the treatment for H. pylori

A

antacids and antibiotics

174
Q

what kind of diseases are the leading cause of death worldwide in children < 5 years old

A

diarrheal diseases

175
Q

how are diarrheal disease transmitted

A

by ingestion of contaminated food or water
- transmitted via fecal-oral route from food or water contaminated with animal or human feces

176
Q

what are the moderate dehydration signs of diarrhea

A
  • thirst
  • restless behaviors
  • decreased urine output
  • sunken eyes, tears absent, decreased moisture in mouth
177
Q

what are the severe dehydration signs of diarrhea

A
  • lethargy, floppy, weak
  • lack of urine output
  • dry mouth
  • poor skin turgor
  • hypovolemic shock
178
Q

what is the treatment and prevention of diarrhea

A
  • diarrhea is often self-limiting
  • rehydration therapy (IV or oral) used to counteract loss of fluid and electrolytes from diarrhea
    • water alone insufficient; glucose increases
      absorptive capacity of intestine
    • oral rehydration salts (ORS) is glucose plus various
      salts
  • antibiotics usually not helpful
  • sewage treatment, handwashing, chlorinating drinking water are important control measures
179
Q

define bacterial gastroenteritis

A

inflammation of the GI tract due to an infection or toxin; associated with diarrhea, loss of appetite, nausea and/or vomiting

180
Q

gastroenteritis can lead to

A
  • food poisoning aka foodborne intoxication
  • infectious diarrhea
181
Q

what is the pathogenesis of food poisoning

A
  • food contaminated with bacteria
  • ingest preformed exotoxin (ingested bacteria are killed)
  • damage to host tissues by the activity of the exotoxin
182
Q

what is the pathogenesis of infectious gastroenteritis

A
  • food contaminated with bacteria
  • ingest bacteria that colonize the gut
  • damage to host tissues by either bacteria replicating and invading the tissue or by bacteria adhering to the gut lining and secreting exotoxin (toxins are produced in vivo)
183
Q

what are the signs/symptoms of food poisoning, is the onset rapid or slow, is it contagious, and is the recovery rapid or slow

A
  • nausea, vomiting, followed by diarrhea
  • rapid onset within hours after ingestion
  • not contagious
  • rapid recovery
184
Q

what are the causative agents of food poisoning

A
  • s. aureus
  • bacillus cereus
  • c. perfringens
185
Q

when does diarrhea occur

A

when water is not absorbed or when it actually leaves intestinal cells and enters the intestinal lumen

186
Q

describe secretory diarrhea

A
  • often mediated by an enterotoxin
  • if bacterial cause, then the infecting bacteria do not invade
  • causes the “runs”
  • watery diarrhea with loss of electrolytes and fluids from the intestines
  • severe dehydration
  • possibly accompanied by nausea and vomiting
  • usually small intestine
187
Q

describe invasive/inflammatory diarrhea

A
  • typically due to bacteria invading the intestinal mucosa
  • causes “the squirts”
  • mucosal lining of the intestine is inflamed and becomes damaged; intestines can’t absorb nutrients and water
  • frequent, diarrhea containing mucus, pus, and sometimes blood in stool (dysentery)
  • pain on defecation, colitis, and fever may also be present
  • usually large intestine
188
Q

enteric bacteria are gram-negative facultatively anaerobic ____ or ____ (curved rods)

A

rods or vibrio

189
Q

how are bacterial infections of the LDS transmitted

A

fecal-oral transmission

190
Q

intestinal pathogens sensitive to acid usually have ___ (high or low) infectious dose, since most are destroyed by acid

A

high
- generally transmitted by contaminated foods and water

191
Q

acid-resistant pathogens have ___ (high or low) infectious dose

A

low
- transmitted through direct contact (hand to hand) or by contaminated foods and water

192
Q

what are three examples of non-invasive enteric bacteria

A
  • enteropathogenic e. coli (EPEC)
  • enterotoxigenic e. coli (ETEC)
  • vibrio cholerae
193
Q

what are some characteristics of e. coli

A
  • gram-neg bacilli
  • ferments lactose (coliform)
  • many strains part of normal microbiota and act as opportunists
  • some strains have developed virulence through plasmid transfers and are primary pathogens
  • strains groups into various pathovars based on the virulence factors
194
Q

enterotoxigenic e. coli (ETEC) has what syndrome

A

watery diarrhea
- “travelers diarrhea”

195
Q

enteropathogenic e. coli (EPEC) has what syndrome

A

watery diarrhea of long duration, most in infants

196
Q

enterohemorrhagic e. coli (EHEC) has what syndrome

A

bloody diarrhea
- hemorrhagic colitis and hemolytic uremic syndrome (HUS)

197
Q

enteroinvasive e. coli (EIEC) has what syndrome

A

blood diarrhea

198
Q

describe EPEC

A
  • non-invasive pathovar of e. coli
  • does not produce toxins
  • changes the microvilli of small intestines -> formation of attaching and effacing lesion
  • prevents reabsorption of water into the cell
199
Q

describe ETEC

A
  • attaches to but does not invade surface epithelium of small intestine
  • mediated by enterotoxins such as heat-labile enterotoxin (LT) which is an A-B exotoxin
200
Q

what is the pathogenesis of ETEC

A
  • LT binds to a receptor and activates adenylate cyclase
  • adenylate cyclase produces elevated levels of cAMP
  • elevated levels of cAMP cause cells to secrete excessive amounts of fluid and electrolytes into the lumen of the intestinal tract
201
Q

what is the reservoir for ETEC, does it have a high or low infectious dose, it is endemic in what kind of countries, who are the at-risk groups, and what kind of diarrhea

A
  • humans are the reservoir
  • high infectious dose
  • endemic in resource-limited countries
  • children <5 years and travelers from non-endemic countries
  • watery diarrhea
202
Q

describe vibrio cholerae (shape, most common source, high or low infectious dose, invasive or non-invasive)

A
  • gram-neg curved rods
  • fecally contaminated water is the most common source
  • high infectious dose
  • non-invasive
203
Q

what does vibrio cholerae cause

A

cholera
- secretory diarrhea

204
Q

describe cholera toxin

A
  • encoded by a bacteriophage
  • A-B toxin
205
Q

describe cholera disease

A
  • depending on the strain, can be mild and self-limiting or very severe and life-threatening
  • copious amounts of watery stool called “rice water” stool
    • up to 20L a day
206
Q

describe cholera in children

A
  • may lost 50% of body weight over the course of an infection
  • dehydration, lethargic, sunken eyes, flaccid skin -> hypovolemic shock -> death
207
Q

what is the treatment for secretory diarrhea

A
  • rehydration therapy is essential
    • IV (intravenous)
    • oral rehydration solution (water, glucose,
      electrolytes)
  • may also treat with antibiotics (eg highly virulent cholera strain)
  • prevention: sanitation and safe water supplies
208
Q

describe enteroinvasive e. coli (EIEC)

A
  • invades and replicates within the mucosa of the large intestine
  • moves from cell to cell via nucleating actin filaments
  • elicits inflammatory response
  • neutrophils damage and ulcerates the intestinal lining
  • dysentery
209
Q

describe enterohemmorhagic e. coli (EHEC)

A
  • strains capable of causing epidemics
  • most commonly identified EHEC in NA is E. coli 0157:H7 strain (O and H refer to surface antigens)
  • invasive pathovar
  • reservoir: ruminant animals (especially cattle)
  • zoonotic
  • typically associated with consumption of undercooked ground beef and raw green leafy veggies contaminated with cattle feces
  • low infectious dose
210
Q

describe shiga toxin (Stx) in e. coli

A

phage-encoded toxin
- A-B type exotoxin
- A subunit inhibits protein synthesis by acting on the rRNA of large ribosome -> lysis -> inflammation
- may travel by blood to the kidney

211
Q

what are some symptoms of EHEC and possible complication

A
  • bloody diarrhea and fatal hemorrhagic colitis
  • possible complication: hemolytic uremic syndrome (HUS)
212
Q

true or false - EHEC is a zoonotic pathogen while ETEC is not

A

true

213
Q

describe shigella

A
  • non-coliform, gram (-) bacilli
  • humans are the reservoir
  • low infectious dose
  • invasive
214
Q

how is shigella transmitted

A
  • self inoculation from fecally contaminated hands
  • ingestion of fecally contaminated foods
  • person-to-person contact from fecally contaminated hands
215
Q

children under 5 are 10 times more likely to contract which disease

A

shigella

216
Q

describe shigellosis (bacillary dysentery)

A
  • abdominal pain, fever
  • bloody diarrhea with mucus and pus
  • straining to defecate
  • complications: febrile seizures, confused and other neurological complications may appear in children
217
Q

what does the blood, mucus, and pus suggest
- colonization of the colonic mucosa without invasion
- secretion of toxin that enters the colonic mucosa and disrupts electrolyte transport
- inflammatory invasion of the colonic mucosa

A

inflammatory invasion of the colonic mucosa

218
Q

describe shiga toxin (Stx)

A
  • the genes for Stx in S. dysenteriae are located on the chromosome
  • A-B toxin that inhibits protein synthesis by attaching the rRNA of the large ribosomal subunit
  • HUS is not as common with shigella as with EHEC
219
Q

describe salmonella enteritidis

A
  • non coliform, gram (-) bacilli
  • high infectious dose
  • invasive
  • does not produce Stx or actin tails like shigella
  • reservoir: poultry (main) - zoonotic
220
Q

how is salmonella enteritidis transmitted

A
  • most human infections due to consuming food contaminated with animal feces
    • especially undercooked poultry and eggs
221
Q

is salmonella more or less sensitive to stomach acid as shigella

A

more sensitive

222
Q

describe salmonellosis

A
  • inflammatory diarrhea, usually mild and non-bloody
  • nausea, vomiting
  • most healthy individuals recover without treatment within 4-7 days
223
Q

who are the high risk groups for severe salmenollosis

A
  • children <5 years, elderly, immunosuppressed adults
  • they require antimicrobial therapy to treat the infection
224
Q

true or false - salmonella remains the leading cause of food-borne fatalities in the U.S.

A

true

225
Q

describe campylobacter jejuni

A
  • gram (-) spiral shaped or curved (vibrio) rods
  • low ID
  • invasive
  • animal reservoir: poultry
  • most common cause of bacterial diarrhea in the US
226
Q

how is campylobacter jejuni transmitted

A
  • poultry is common source of infection
  • raw chicken fluids cross contaminate uncooked food
  • campylobacter can be cultured from 60-100% of chickens purchased in supermarkets
  • zoonotic
227
Q

describe campylobacteriosis

A
  • fever, nausea/vomiting
  • watery diarrhea that transitions into inflammatory diarrhea with abdominal pain
  • dysentery occurs in about half the cases
  • complications include: irritable bowel syndrome and guillain barre syndrome (temp nerve paralysis)
228
Q

true or false - a case of bacterial inflammatory diarrhea progresses to severe colitis

A

true

229
Q

describe c. diff shape

A
  • gram (+)
  • obligate anaerobe
  • spore-former
230
Q

how is c. diff transmitted

A

usually by contact with contaminated health care worker’s hands
- resistant to many antibiotics
- opportunistic pathogen

231
Q

enterotoxins (A and B) bind to intestinal epithelial cells and do what two things

A
  • kills mucosal epithelial cells
  • inflammation, diarrhea
232
Q

describe pseudomembranous colitis

A
  • caused by enterotoxins that cause necrosis of the epithelial cell lining the colon
  • dead epithelial cells, exudate, dead neutrophils, and bacteria form pseudomembranes
  • bloody diarrhea and abdominal pain
233
Q

can you treat c. diff with fecal microbiota transplants (FMT)

A

yes

234
Q

what three toxins cause food poisoning

A
  • s. aureus
  • bacillus cereus
  • c. perfringens
235
Q

describe bacillus cereus causing food poisoning

A
  • gram (+)
  • endospore-forming
  • facultative anaerobe
  • soil bacterium
  • transmission: via ingestion of toxin-contaminated food
  • associated with rice
236
Q

b. cereus enterotoxin acts as a

A

superantigen

237
Q

describe c. perfringens causing food poisoning

A
  • gram (+)
  • endospore-forming
  • obligate anaerobe
  • found in soil but also cows and poultry
  • transmission: via ingestion of toxin-contaminated food
  • associated with beef or poultry
  • outbreaks often happen in hospitals, prisons, nursing homes “food service germ”
238
Q

describe viral gastroenteritis

A

transmission: fecal-oral route
- more than 95% of viral gastroenteritis hospitalizations occur in children under the age of 5

239
Q

describe rotavirus

A
  • most common cause of infantile gastroenteritis
  • nearly all unvaccinated children infected before age 5
  • reservoir: humans
240
Q

describe the rotovirus

A
  • naked virus
  • transmission: fecal-oral route
  • begin abruptly with vomiting and slight fever, followed shortly by profuse watery diarrhea
  • usually clears within a week, but fatal dehydration can occur if fluids are not replaced
241
Q

what is the vaccine for rotovirus

A
  • oral rotavirus vaccine
  • live attenuated vaccine
242
Q

true or false - the most common viral cause of diarrhea in adults and the second most common viral cause of diarrhea in children (after rotavirus) is norovirus

A

true

243
Q

what are the signs/symptoms of norovirus

A
  • abrupt onset of explosive vomiting and watery diarrhea
  • resolves after 24-48 hours
244
Q

describe cyst (protozoan disease of LDS)

A
  • non-replicating, dormant
  • infectious
  • resistant
  • outside of host
245
Q

describe trophozoite (protozoan disease of LDS)

A
  • feeding and reproducing life form
  • inside the host
246
Q

describe giardia lambia

A
  • intestinal protozoan with cyst and trophozoite forms
  • moves via flagella
  • transmitted fecal-oral route; waterborne
  • beavers are a major reservoir
  • zoonotic
247
Q

true or false - giardiasis is the most commonly identified waterborne illness in the US and is associated with hikers drinking from the streams

A

true

248
Q

what are symptoms of giardiasis

A
  • non-invasive watery (secretory) diarrhea lasting 1-4 weeks
  • fatty (greasy appearance), smelly watery diarrhea
  • flatulence
  • malnutrition (severe cases)
  • about 50% of infections are asymptomatic carriers (cyst passers)
249
Q

how to diagnose giardiasis

A
  • a stool ova and parasite exam involves direct examination of a stool sample for the presence of cysts and trophozoites
  • can be used to distinguish common parasitic intestinal infections
  • ELISA and other tests are used
250
Q

describe cryptosporidium parvum

A
  • protozoan parasite
  • reservoir: cattle
  • causes cryptosporidiosis
  • transmission via ingestion of water contaminated with animal feces (drinking water or swimming)
251
Q

what is an oocyst

A

protected by a thick outer shell that allows it to survive outside the body for long periods of time and makes it very tolerant to chlorine disinfection

252
Q

describe cryptosporidiosis

A
  • non-invasive, secretory (eg watery) diarrhea
  • self-limiting in immunocompetent persons (lasts 10-14 days)
  • severe unrelenting and life-threatening diarrhea in immunocompromised hosts (AIDS)
253
Q

how to diagnose cryptosporidiosis

A

ova and parasite exam: modified acid-fast staining of stool

254
Q

describe shape of enterobius vermicularis

A
  • helminth
  • small (length of a staple) intestinal roundworm called pinworm
255
Q

what is the enterobiasis epidemiology

A
  • most common helminth infection in the U.S. usually in children
  • transmitted via fecal-oral route
  • reservoir: humans
256
Q

enterobiasis symptoms

A
  • eggs are very sticky and itchy
  • perianal pruritis
  • sleeplessness

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