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Module 3: CPR > Microbiology II > Flashcards

Microbiology II Flashcards

1
Q

What pathogens can be found at the nasopharynx?

A

Mainly viruses

  • rhinovirus
  • coronavirus
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2
Q

What pathogens can be found at the oropharynx?

A

Strep pyogenes (Group A Strep)

Corynebacterium

Diphtheriae

Epstein-Barr virus

adenovirus

enterovirus

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3
Q

What pathogens can be found in the middle ear and parasinuses?

A

Strep pneumoniae

Haemophilus influenzae (non-typeable)

Moraxella catarrhalis

Group A Strep

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4
Q

What pathogens can be found on the epiglottis?

A

Haemophilus influenzae Type b

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5
Q

What are characteristics of Group A Strep?

A

Streptococcus pyogenes

  1. Gram + cocci in chains
  2. Catalase negative
  3. Beta-hemolytic
  4. Bacitracin sensitive
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6
Q

What are symptoms of pharyngitis and what is the most notable cause of pharyngitis?

A

Symptoms:
nausea
vomiting
abdominal pain

Complications:
peritonsillar abscesses
scarlet fever
cervical adenitis
otitis media
strep. TSS

Group A Strep

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7
Q

How does Group A Strep cause rheumatic heart disease?

A

M protein is a virulence factor of S. pyogenes that allows it to go undetected by the immune system due to its molecular mimicry of cardiac proteins

S. pyogenes infections can lead to anti-cardiac antibodies produced by the immune system

These antibodyes are responsible for deposits and thickenign of leaflets leading to RHD

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8
Q

What are characteristics of Haemophilus Influenzae bacteria?

A

Gram -

Coccobacilli
(curved ends on short rods)

Oxidase positive

Growth Requirements:
Fastidious
X Factor (hemin, heat stable)
V Factor (NAD or NADP, heat labile)

Grown on Chocolate agar

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9
Q

What is the most agressive capsular type of H. Influenzae? Why?

A

H. influenzae Type b
(HIb)

Type b capsule is polyribose-ribitol phosphate

Capsule is:
Antiphagocytic

Non-encapsulated forms are normal flora in the URT

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10
Q

What are types of diseases are caused by H. influenzae?

A

Meningitis - 90% die w/o treatment

Epiglottitis - obstructive, cherry red epiglottis, life threatening

Pneumonia - often complicated by empyema

Bacteremia

Cellulitis

Septic arthritis

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11
Q

What infections are caused by non-typeable H. influenzae?

A

Acute otitis media

sinusitis

  • may follow viral infection

Exacerbations of COPD

Conjuctivitis (daycare settings)

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12
Q

What is treatment for H. influenzae?

A

3rd generation Cephalosporin

If susceptible to ampicillin, use that

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13
Q

Why must polysaccharide vaccines be protein conjugated for children?

A

Infants cannot make antibody responses to polylysaccharides because they are T-independent antigens.

The conjugate vaccine allows the infant to make an antibody response (and evoke memory cells) because the protein part of the conjugate engages T cells and allows the polysaccharides to be presented as T-dependent antigens.

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14
Q

What is the causative agent of diptheria?

A

Corynebacterium diphtheriae

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15
Q

What are characteristics of Corynebacterium diptheriae?

A

Gram + rods
(“chinese letters”)

catalase +

non-motile

non-spore forming

Produce diptheria toxin in mucus membranes

Produce Pseudomembranes that may occlude airway

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16
Q

What is the pathogenesis of diphtheria?

A

Organisms enter URT –> Colonize mucose –> Produce diptheria toxin

Diptheria toxin causes:

Myocarditis

Neuritis

Necrosis
(causes pseudomembrane)

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17
Q

What is Diptheria toxin?

A

Toxin produced by Corynebacterium Diptheriae that is encoded on a lysogenic phage (can be transduced to other corynebacterium species)

Three domains:

A = active domain
B = binding domain
T = transmembrane domain

Mode of Action:

Inhibits protein synthesis and kills cells

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18
Q

What is treatment for Corynebacterium Diptheriae infections?

A 
**Antitoxin** to treat diptheria toxin
 Horse origin (test for sensitivity)

Antibiotic to eradicate organisms

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19
Q

What are the characteristics of rhinovirus?

A

Non-enveloped

+ssRNA genome

Icosahedral capsid

Small in size

>100 serotypes

ICAM-1 is primary cellular receptor used to infect respiratory epithelial cells

Temperature Sensitive
88-90deg F

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20
Q

How is rhinovirus transmitted?

A

aerosol droplets
(sneezing)

direct contact with infected surface

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21
Q

What is the rhinovirus replication cycle?

A

Cytoplasmic:

Rhinovirus binds to ICAM-1 –> enters epithelial cell

+ssRNA is translated by cell’s ribosomes

+ssRNA is transcribed by virus’s RNA polymerase

Proteins and RNA are assembled

Virus exits by Lysis of cell

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22
Q

What are symptoms of rhinovirus? How long do they last?

A

Infection of about 2-4 days (self-limiting)

Symptoms:

Nasal discharge
Nasal congestion
Sneezing
Sore throat
Edema and erythema of nasal mucosa
Muscle aches
fatigue
headache
loss of appetite

In rare cases of children: bronchopneumonia

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23
Q

How does someone become immune to rhinovirus?

A

No Vaccines

Mucosal IgA in nasal secretions are protective

Type I interferons control viral spread but causes pathogenesis

Immunity is serotype specific
>100 serotypes

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24
Q

At what point does a Respiratory Syncytial Virus infection become life threatening?

A

Primary infection occurs in epithelial cells of URT producing a mild, self-limiting illness

In children <8 months old, virus can spread to LRT, causing:
Bronchitis
Pneumonia
Croup

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25
Q

What are characteristics of Respiratory Syncytial Virus (RSV)?

A

Enveloped

-ssRNA genome

Helical Capsid

Two major envelope proteins:
Attachment (G) protein
Fusion (F) protein

Aggregated F proteins cause syncitia

Encodes its own RNA-dependent-RNA Polymerase

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26
Q

What is the RSV replication cycle?

A

Cytoplasmic
It’s a -ssRNA virus that causes cytoplasmic inclusion bodies:

RNA is transcribed by the virus’s RNA-dependent-RNA polymerase

Then RNA is translated into proteins

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27
Q

How is RSV diagnosed?

A

NAsal washings, nasal aspirates or swab samples are useful for antigen detection

Rapid diagnosis by:
DFA
IFA
ELISA

Viral culture is carried out in cell lines

Molecular assays such as RT-PCR

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28
Q

How is RSV treated?

A

No liscenced vaccine

Ribavirin has been used but has limited efficacy

Oxygen treatment and hospitalization for infants with severe brochiolitis

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29
Q

What passive immunotherapy is used against RSV?

A

RespiGam: polyclonal antibody used to prevent serious LRT infection for infants and bone marrow recipients

Synagis: monoclonal antibody (anti-F reactive Ab) for pediatric patients at high-risk of RSV (i.e. babies on ventilators)

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30
Q

What virus is known to cause outbreaks on epidemic levels for military training centers?

A

Adenovirus

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31
Q

What are characteristics of adenovirus?

A

Non-enveloped virus

ds linear DNA

Icosahedral capsid

51 known serotypes

Replicates in nucleus

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32
Q

What are the phases of adenovirus replication?

A

In nucleus:

Immediate early:
E1A genes transcribed

Early:
E1B, E2A, E2B, E3, E4, some virion proteins transcribed

Late:
Late genes, mostly virion proteins

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33
Q

What proteins allow for adenovirus to be infectious?

A

Hexon and Penton bases extend fibres out of the capsid

–> attach to cells and activate viral infection

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34
Q

What respiratory diseases are caused by adenovirus?

A
  • Febrile, undifferentiated URI
  • Pharyngoconjunctival fever
  • Acute respiratory disease
    (military recruits)
  • Pertussis-like syndrome
  • Pneumonia
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35
Q

How is immunity of adenovirus mediated?

A
  • *Humoral:**
  • neutralizing Ab’s are protective against some serotypes

Cell-mediated:
CD8 CTL responses are critical in controlling infection

  • severe infections are common in people with cellular immune defects

Adenovirus encodes proteins that play role in immune invasion:

  • down regulates MHC class I
  • inhibits TNF mediated lysis
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36
Q

How is adenovirus diagnosed?

A

Detection of Antigen:
Rapid diagnosis from nasopharyngeal aspirates or throat washings

Virus Isolation

Serology

PCR Assays

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37
Q

How is adenovirus treated?

A
  • Symptomatic treatment
  • Self-limiting: 7-10 days
  • new live tablet vaccine approved in 2011 used by military during basic training
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38
Q

What classification of virus is Epstein Barr?

A

gamma Herpesvirus:

  • restricted host-range
  • infects epithelial cells and lymphocytes
  • latent in lymphocytes and/or endothelial cells
  • can cause cancer
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39
Q

What are characteristics of EBV?

A

All Herpesviruses have identical morphology:

Enveloped

linear dsDNA

Icosahedral capsid

encodes its own DNA-dependent DNA pol

encodes numerous host protein homologues to evade immune responses

replicates in nucleus

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40
Q

What does EBV infection cause? What are the symptoms?

A

Infectious mononucleosis

Symptoms:

Fatigue
Malaise
Throat soreness and reddening
Tonsil reddening, swelling, white patches
Cervical adenopathy

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41
Q

What about EBV is thought to be the cause of cancer?

A

EBV latency

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42
Q

How is infectious mononucleosis diagnosed?

A
  1. Atypical lymphocyte
    (Downey cells = CD8 CTL)
  2. Agglutination test for heterophile Abs
    (using fresh horse or sheep RBCs)
  3. EBV Ab ELISA
  4. PCR for EBV genes
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43
Q

How is EBV treated?

A

No vaccine:

Symptomatic treatment

Infectious Mononucleosis is self limiting

  • rapidly controlled by immune response
  • symptoms can linger for weeks
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44
Q

What are the major components of mycobacterial cell envelopes?

A

Waxes

Mycolic acids

polysaccharides

peptidoglycan (murein)

Phenolic Glycolipid I (PGL-1)

Lipoarabinomannan (LAM)

–> Acid Fast staining

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45
Q

What is the pathogenesis of TB?

A

Infectioin that requires cell-mediated immunity for control

  • Ab response is not effective

No toxins involved

There is an active and latent
infection does not mean disease

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46
Q

What is the life cycle of M. tuberculosis?

A
  1. Mycobacterium enters alveoli and infects alveolar macrophage
  2. Infected macrophages release cytokines attracting monocytes, further spreading infection
  3. Immune cells wall of the site of infection with a fibrouls cuff, encapsulating bacilli, foamy macrophages, and the center becomes a necrotic, caseatign granuloma
  4. The granuloma can burst, further spreading infection
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47
Q

How can M. tuberculosis infection lead to disease?

A

Infection of the alveoli in people with little to no hypersensitivity/cell-mediated immunity (immune-compromised) become infected with a progressively systemic disease and eventually death

Infection in people with DTH and CMI –> disease is contained; bacteria live but fail to replicate –> Ghon complex appears in 15% of cases

Ghon complex appears >5 years later in 25% of cases

  • leading to:
    progressive systemic disease and death,
    clinical TB (pulmonary or extrathoracic)
    or
    no disease
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48
Q

How does reactivation of TB occur?

A
  • viable bacteria w/in lesions are the source of reactivation
  • Usually found in upper lung
  • Triggers:
    Diminished immune response
    Malnutrition
    Aging
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49
Q

What is a Ghon complex?

A

Some individuals develop the Ghon complex in primary infection of TB in which:

an area of lung inflammation is associated with enlarged hilar lymph nodes

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50
Q

What people are at higher risk of being exposed to TB?

A
  • Persons in close contact w/someone w/known or suspected TB infection
  • Foreign-born persons from areas known to have TB
  • Residents & employees of high risk congregate settings (i.e. nursing homes)
  • Health care workers who serve high risk clients
  • Medically underserved, low-income populations
  • high risk racial or ethnic minority
  • persons who inject illicit drugs
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51
Q

What people are at higher risk of developing TB disease once infected?

A
  • HIV infected
  • recently infected
  • persons with certain medical conditions
  • persons who inject illicit drugs
  • History of inadequately treated TB
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52
Q

How is TB diagnosed in the laboratory?

A
  • Sputum smear - need minimum of 10^4 bacilli/ml for + smear
  • culture (“gold standard”) - slow, takes 2-3 weeks to form colony
  • Tuberculin skin test (PPD or Mantoux)
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53
Q

What is a PPD test?

A

Purified Protein Derivitive (Of Tuberculosis)

  • intradermal injection of purified protein

+ test produceswheal 6-10mm in diameter
(diameter of + test depends on risk of patient)

reaction must be read in 48-72hrs

54
Q

What can cause a false-positive PPD?

A

Nontuberculous mycobacteria

BCG vaccination

55
Q

What can cause a false-negative PPD?

A

Anergy
(lack of rxn by the body)

Recent TB infection

Very young age (<6 mo. old)

live virus vaccination

overwhelming TB disease

56
Q

Why is it important to culture TB?

A

it is required to isolate bacteria for:

drug susceptibility testing
(deterine best route of treatment)

genotyping

57
Q

How is TB treated?

A

Generally in drug combinations: Isoniazide, Pyrazinamide, Rifampin

First line drugs:
Isoniazid
Pyrazinamide
Rifampin
Rifapentine
Ethambutol

Second line drugs:
Cycloserine
Ethionamide
Streptomycin
(many more)

58
Q

What is BCG?

A

Bacile de Calmette et Guerin

  • Live, attenuated vaccine for TB derived from Mycobacterium bovis

Not used in US b/c:

  • adverse rxns
  • Immunity wanes in ~10yrs
  • Interferes w/use of PPD
59
Q

What is the pathogenesis of Influenza?

A

Primary Infection

Secondary infection
(re-infection)

60
Q

What is the development of primary infection of influenza?

A
  1. Short incubation period
  2. local virus replication in respiratory epithelium
  3. damages to epithelium and ciliated columnal epithelial cells (renders airway susceptible to bacterial infection)
  4. No viremia
  5. macrophage and lymphocyte infiltrate
  6. interferon and cytokines cause fever, aches, edema
  7. direct virus damage and immmune response kill infected cells
  8. Stimulation of Abs and virus-specific T cells
  9. Clearance of virus from tissues
  10. immunity mediated by IgA in respiratory tract
61
Q

What are clinical features of influenza?

A
  • Abrupt onset of symptoms:
    headache
    fever
    chills
    myalgia
    malaise
    sore throat
    non-productive cough
    runny or stuffy nose
62
Q

What are characteristics of the Influenza Virus?

A

neg. RNA virus (segmented RNA)

Enveloped

Haemagglutinin (HA) and Neuraminidase (NA) spikes

3 types: A, B, C

63
Q

What are complications of influenza?

A

Secondary bacterial pneumonia:
following improvement, fever reappears, cough, purulent sputum

Viral pneumonia:
Relentless progression of illness, dyspnea, hypoxia, cyanosis, severe inflammatory reaction in alveoli, edema –> ARDS

Myositis and cardiac involvement

Neurologic symptoms
(Guillain-Barre syndrome, encephalopathy, encephalitis, Reye’s syndrome)

64
Q

What are the three types of Influenza virus?

A

Type A: Undergoes antigenic shift and drift

Type B: undergoes antigenic drift only

Type C: relatively stable, doesn’t cause serious human disease

65
Q

What is the purpose of Haemagglutinin and neuraminidase on influenza viruses?

A

HA: viral attachment and membrane fusion
HA1/HA2 binding site (a disulfide bond) must be cleaved for infection to expose fusion peptide

NA: virus release from infected cells and disaggregation

66
Q

How does replication occur for influenza virus?

A
  • Virus binds sialic acid moiety on glycoproteins and glycolipids
  • transcription and replication occur in nucleus
    (virus includes its own RNA-dependent RNA pol)
  • Steal 5’ capped termini of cellular mRNAs as primers for virla mRNA transcription
  • Budding from plasma membrane
  • frequent genetic reassortment occurs
67
Q

How is influenza diagnosed?

A
  • samples obtained from respiratory secretion
    (throat swab, nasal wash, throat wash, nasopharyngeal aspirate)
  • Virus grown in fertilized eggs or in cell cultures
  • Detect virus replication by cytopathic effects, immunofluorescence, hemagglutination, or hemadsorption
  • determine serotype by hemagglutination-inhibition test
  • or rapid diagnoisis by RT-PCR based tests
68
Q

What is antigenic shift?

A

Occurs as a result of the segmented genome of flu virus and reassortment of viral genomes in the large animal reservoirs of the virus

69
Q

What is antigenic drift?

A

Occurs as a consequence of the mutations introduced by viral RNA dependent RNA polymerase during replication of flu virus

70
Q

What are the two vaccine types used against influenza?

A

Trivalent Inactived Vaccine:
2 Type A, 1 Type B
Chemically inactived vaccine
Induces serum antibodies

Live Attenuated Influenza Vaccine:
2 Type A, 1 Type B, nasal spray
Induced mucosal immunity

71
Q

What do antiviral therapies for influenza target?

A

Neuraminidase: (responsible for virus release from cell)
Oseltamivir
Zanamivir

Ion Channel (M2): (facilitates virus dissembly and HA maturation)
Amantadine
Rimantadine

72
Q

What is Amantadine and Rimantadine?

A

Antiviral therapies for influenza

  • blocks Ion channel activity of M2 protein
  • prevents H+ entry into viral interior thereby inhibiting viral dissembly
  • also inhibits maturation of HA during virus assembly
  • **reduces disease severity only if given early
  • only for Type A Influenza**
73
Q

What is the function of M2 in influenza life cycle?

A
  1. lowers the pH in virla particle to facilitate dissociation of the ribonucleoprotein complexes form the M1 protein
  2. facilitates HA maturation and egress by equillibrating pH of Golgi and cytoplasm during assembly
74
Q

How is pneumonia classified?

A

It is an infection of the lung parenchyma

  • Acute*: Fairly sudden onset with progession of symptoms over a few days
  • Community Acquired
  • Hospital Acquired (think Gram- rods)

Subacute or Chronic

75
Q

What is a “typical” pneumonia?

A

high fever

shaking chills

chest pain

lobar consolidation on CXR

76
Q

What are common causes of Typical pneumonia?

A
  • Strep. pneumoniae (community acquired)
  • Staph. aureus (CAP)
  • Haemophilus influenzae (CAP)
  • Gram - enterics (hospital acquired)
77
Q

What is an “atypical” pneumonia?

A

less severe illness (“walking pneumonia”)

Insidious Onset

Dry cough

headache

other systemic complaints

CXR diffuse pattern: looks worse than symptoms suggest

78
Q

What are common causes of “atypical” pneumonia?

A

Mycoplasma pneumonia

Chlamydia pneumonia, psittaci

Legionella pneumophila

Influenza, or other virus

Coxiella burnetti

79
Q

What are characteristics of Strep. pneumoniae?

A

Gram +, lancet shaped cocci

Catalase negative

Alpha-hemolytic

Diplococcus bacteria

Sensitive to optichin

Bile soluble (Enzymes cause lysis of colony in bile salts)

Colonies are mucoid b/c of capsule

80
Q

What is a major virulence factor of Strep. pneumoniae?

A

Capsular polysaccharides:

Capsule interferes with deposition of C3b on bacterial surface

Therefore, no recognition of C3b-coated organisms by complement receptors on phagocytes

**Anti-capsular Abs provide type-specific immunity

81
Q

What are risk factors for Strep. pneumoniae?

A

Viral infection of URT
(particularly influenza)

Compromised pulmonary function
(alcoholism, general anesthesia)

Age
(elderly or <2)

Ethnicity
(blacks, American indians, alaska natives)

Basic immunity impaired

Serotype of S. pneumoniae present in URT

82
Q

What is the pathogenesis of pneumococcal pneumonia?

A

Organism colonizes pharynx and gains access to lung/alveoli

Phagocytized by macrophages (stops infection)
OR
Multiplys in edematous fluid (continues infection)

Exudate spills into bronchiles and adjoining alveoli

Inflammatory response, air displaced

Centrifugally spreading lesion leads to resolution or death

83
Q

What are signs and symptoms of pneumococcal pneumonia?

A
  • It’s usually lobar –> oldest part of lesion in center
  • sudden onset of fever, chills, pleuritic pain, rusty sputum
  • positive blood cultures
84
Q

What are possible complications of pneumococcal pneumonia?

A

Direct:
lung abcess

Via blood:
empyema
pericarditis
meningitis
intrapleural abscess
septic arthritis

85
Q

What is the therapy for pneumococcla infections?

A

Many isolates of Strep. pneumoniae are now penicillin resistant

  • no distinct drug regimen
  • Conjugate vaccine is available for prevention
86
Q

What bacterial agents commonly cause atypical pneumonia?

A

Mycoplasma pneumoniae

Chlamydia pneumoniae

Chlamydia psittaci

Coxiella burnetti

87
Q

What are common viral agents of atypical pneumonia?

A

Adenovirus

parainfluenza virus

EBV

RSV

88
Q

What are characteristics of Mycoplasma bacteria?

A

Lack cell wall (no peptidoglycan)
–> no target for antibiotics

Unit membrane containing sterols

Pleomorphic

too small to filter out

Facultative aerobes (except M. pneumoniae)

Grow slowly

Reproduce via binary fission

89
Q

What is the pathogenesis of M. pneumoniae?

A

Entry via respiratory route

  • *Bacteria attach to epithelial cells of LRT**
  • tight association, but no invasion
  • Bacterial attachment factor: P1 adhesin
  • Cell membrane receptor: neuraminic acid-containing glycoprotein

Induction of ciliostasis
Deterioration of cilia in respiratory epithelium, both structurally and functionally
Caused by production of Community Acquired Respiratory Distress Syndrome toxin (CARDS toxin)

Bacteria are phagocytized by activated macrophages; cytokine production –> local inflammation

Vigorous CMI –> severe clinical case

90
Q

How is M. pneumoniae diagnosed?

A
  • Diagnosis of elimination
  • Culture: very difficult; restricted to specialized labs
  • Serology: >4-fold rise in specific M. pneumoniae Ab
  • Test for Cold hemagglutinins (not specific)
91
Q

What are cold hemagglutinins?

A

IgM antibodies that bind I antigen of human RBCs produced in 1-2 weeks after initial infection (i.e. M. pneumoniae)

–> able to agglutinate RBCs at 4deg C

92
Q

What is the treatment for Mycoplasma pneumoniae?

A
  • Antimicrobial therapy shortens period of symptoms
  • Antibiotics of choice:

Tetracycline
Erythromycin or azithromycin
beta-lactams NOT effective (no cell wall)

  • No vaccine available
93
Q

What are the characteristics of Chlamydiaceae?

A
  • Enveloped
  • Obligate intracellular bacteria
  • Contain DNA, RNA, and 70s Ribosomes
  • divide by binary fission
  • carry plasmids; infected by bacteriophage
  • Similar to Gram (-) bacteria, but no detectable peptidoglycan
    (sensitive to cell wall antibiotics)
94
Q

What are the developmental forms of Chlamydia?

A

Elementary Bodies:
Extracellular
Infectious form
metabolically Inactive
Disulfide cross-linked outer membrane proteins

Reticulate Bodies:
Intracellular
Replicative form
Metabolically Active
Osmotically fragile

95
Q

How does Chlamydia enter the cell?

A 
Elementary bodies (infectious form) enter through
 "Parasite-specified endocytosis"
  • Rapid internalization through receptor-mediated Clathrin-coated endocytosis
96
Q

How is C. pneumoniae Pneumonia diagnosed?

A

Culture: difficult; restricted to specialized labs

Serology: IgM titer of >= 1:64
or 4-fold rise in IgG in acute and convalescent serum, measured 4 weeks apart

–> have to wait for recovery for diagnosis

97
Q

What is an increased risk factor for Chlamydia psittaci?

A

Working with Birds: poultry industry workers, vets, exotic bird owners

–> Zoonotic infection:
“Parrot fever” - wasting disease of birds
Spontaneous abortion in sheep (and humans)

98
Q

What are clinical features Psittacosis and how is it transmitted?

A

Clinical Features:

Abrupt onset

Fever, headache, myalgia, mild cough

abnormal Chest exam

Confusion/altered concious state

Transmission:

Inhalation of aerosolized organism in dried feces or respiratory tract secretions

direct contact with infected bird

99
Q

How is psittacosis diagnosed and treated?

A

Diagnosed through culture of C. psittaci from respiratory tract or serology

Treatment:
Doxycycline
macrolides (azithromycin, erythromycin)

100
Q

What are risk factors for Legionnaire’s disease?

A

Immunosuppression

Cigarette smoking

renal failure

Age > 50yrs

AIDS

hematologic malignancies

lung cancer

Males > women

101
Q

What are characteristics of Legionella?

A

Gram (-) slender bacilli
–> don’t take Gram stain well

Specific growth requirements:
Amino acids
Iron and other trace metals
–> Buffered Charcoal Yeast Extract Agar

Slow growing

L. pneumophila predominant species in human disease

102
Q

How is legionella spread?

A
  • most commonly spread through aerosols
  • A/C cooling towers
  • Whirlpool spas
  • sink taps and shower heads
  • replicates anywhere btwn 5deg and 63deg C
  • loves biofilms
103
Q

How does legionella infect it’s host?

A

Ameobas or Macrophages:
“coiling phagocytosis” - special mechanism of uptake of legionella

  • Phagosome does not acidify, does not fuse w/lysosome
  • Phagosome surrounded by ER studded with ribosomes
  • Legionella multiplies in phagosome
  • phagosome ruptures
  • host cell lyses, bacteria escape
104
Q

What is Pontiac Fever?

A

Form of Legionellosis in Pontiac, MI:

Influenza-like

  • fever, chills, myalgia, headache
  • no evidence of pneumonia
  • self-limiting
  • no agent cultured
  • retrospectively determined to be legionella
105
Q

What are the approaches to diagnosing Legionellosis?

A
  1. Urine sample
    - LPS antigen detectable by ELISA
  2. Bronchoalveolar lavage (broncheolar machrophages)
    Fluorescence staining on specimens
    or
    Dieterle’s Silver Stain instead of gram stain
    or
    DNA probes on specimens
    or
    Culture on Buffered Charcoal yeast extract agar
  3. Acute and convalescent sera
    - 4-fold Ab rise
106
Q

What is the treatment for Legionella?

A

Macrolides:
Azithromycin, Erythromycin

Fluoroquinilones:
Ciprofloxacin, Levofloxacin

107
Q

What are characteristics of pseudomonas aeruginosa?

A

Gram (-) rods

Flagellated

Strict aerobes

Use oxidative metabolism
NONFERMENTERS

Mucoid capsule makes for a slimy and sticky culture

Oxidase (+)

Growth on MacConkey (Lac -) agar

Pigment production: pyocyanin (green)

Glucose oxidation

Artificial grape-like odor

108
Q

What type of patients are most vulnerable to pseudomonas?

Why?

A

Cystic Fibrosis
–> chronic, recurrent pneumonia

Why:

  • P. aeruginosa infections often become permanent
  • >80% adults with CF are chronically infected
  • P. aeruginosa and other agents for biofilms and become surrounded with breakdown products of bacteria and immune cells
  • Matrix makes bacteria more resistant to both antibiotics and immune system

–> mucous of CF lungs is a perfect place for Ps. to stick to and grow

109
Q

What are the most recognized Ps. aeruginosa diseases?

A
  • pneumonia in CF patients
  • burn infections
  • hospital acquired infections
  • cellulitis
  • folliculitis (hot tub folliculitis)
  • urinary tract infection
  • swimmer’s ear
110
Q

What antibiotics are useful in treating pseudomonas?

A

Aminoglycosides

Carbapenems

Carboxypenicillins

Ureidopenicillins

Extended-spectrum cephalosporins

fluoroquinolones

monobactam

111
Q

What is a dimorphic fungi?

A

Organims that exists as mold in nature and as yeast in vivo

112
Q

What is the morphology of Histoplasmosis?

A

Mold form:
White or brown hyphal colonies

Conidia:
Large spherical ones with spikelike projections
small, oval microconidia

grows slowly, can grown on cycloheximide

Yeast form:
Intracellular

uninucleate

oval

Thin walled

113
Q

How is histoplasmosis spread?

A

Mold lives in soil w/high nitrogen content

  • areas contaminated by bird or bat droppings

Outbreaks are associated with soil disturbances:

  • exposure to caves and bird roosts
  • excavation and demolition of old buildings
114
Q

What is the pathology of histoplasmosis?

A

Spores –> Lungs –> yeast form –> into macrophages –> Reticuloendothelial system (RES)

  • multiply within macrophages
  • travel to hilar and mediastinal lymph nodes
  • spread throughout the entire RES (lungs, LN, liver, spleen, bone marrow)
  • Macrophages become fungicidal –> develop necrosis with fibrous encapsulation (granuloma) –> Ca++ deposition occurs over several years

**Pathophysiologically same as TB

115
Q

What is the most common clinical presentation of histoplasmosis?

A

Asymptomatic
(or just not sick enough to go to the Dr)

116
Q

What are the three pulmonary syndromes common with Histoplasmosis?

A
  • *Acute:**
  • usually mild, self-limiting (10-14d)
  • fever, sweats, cough, occ HA and GI complaints
  • diffuse pulmonary infiltrates and hilar/mediastinal LN involvement

Subacute:
Presents over weeks
- fever, sweats, cough, weight loss
- hilar/mediastinal lymphadenopathy
- possibal focal or patchy pulmonary infiltrate

Chronic:
Inability to clear infection
Same symptoms as subacute

117
Q

What are some ways histoplasmosis infection can present other than pulmonary involvement?
(note these are not completely void of pulm. involvment)

A
  • *Mediastinitis:**
  • freq. complication of pulmonary histo
  • can lead to acute pericarditis and cardiac tampanode

Progressive Disseminated Histo:
- Patients with compromised cell-mediated immunity
and patients on TNFa inhibitors

  • fever, wt loss, sweats
  • hepatosplenomegaly and lymphadenopathy
  • hematologic abnormailities due to bone marrow involvement
  • respiratory distress
  • possible GI, adrenal, CNS, mucosal involvement
118
Q

How are histoplasmosis infections diagnosed?

A

Culture (“gold standard” but slow)

Fungal stain

Serology (doesn’t say if infected, only if they have been infected in their lives)

Antigen (good for disseminated disease)

119
Q

What is the treatment for histoplasmosis?

A

Primary self-limited: none

Moderate disease: Itraconazole

Severe disease: Amphotericin B

120
Q

What is the morphology of blastomycosis?

A

Mold:
White to tan filamentous mold
Round to oval conidia on terminal hyphal branches

Yeast:
Spherical
multinucleated
Thick “double-contoured” walls
Reproduce by formation of buds

121
Q

What is the pathogenesis of blastomycosis?

A

Inhalation of conidia into alveoli –> organisms change to yeast form in lungs –> multiply by budding –> hematogenous dissemination may occur before immunity develops

122
Q

What is the clinical presentation of blastomycosis?

A

Most cases are asymptomatic

Those symptomatic get:

  1. Pulmonary infection: acute pneumonia
  2. Cutaneous: verrucous or ulcerative
  3. Bone: osteomyelitis
  4. Genitourinary: prostatitis and epididymoorchitis
123
Q

How is blastomycosis diagnosed?

A

Histopathology (biopsy)

Culture

Serology (poor specificity)

124
Q

What is the treatment for blastomycosis?

A

Mild disease: itraconazole

Severe disease: amphotericin B

125
Q

What is the morphology of coccidioidomycosis?

A

Mold:
Grows quickly in culture 25deg C

Arthroconidia = funcgal spores that form by segmentation of pre-existing fungal hyphae

Usually barrel-shapped and alternating as they are separated by disjunctor cells

Yeast: (usually in lung)
Arthroconidia become spherules

Spherules produce endospores

Rupture of spherule results in release of endospores, which become new spherules

126
Q

What is the clinical presentation of coccidioidomycosis?

A

Most common: Self-limiting pneumonia
Symptoms: fever, cough, chest pain, fatigue, shortness of breath, chills, muscle and joint aches, night sweats, weight loss
–> can last for several months

  • *Dissemination to skin, bone, and meninges** is possible
  • -> generally afflicts those with immunosuppresion
127
Q

How is coccidioidomycosis diagnosed and treated?

A

Diagnosis:
Direct microscopic eval of sputum

Culture @ 25deg C (must tell lab you think coccidio b/c of possible spreading)

Serology (rising titers is bad prognostic sign)

Treatment:
Mild to moderate: Fluconazole or itraconazole

Severe: amphotericin B

128
Q

What is the morphology of paracoccidioidomycosis?

A

Limited to tropical and subtropical Central and S. America

Yeast form:
variable size

oval to round with multiple buds (“pilot wheel”)

129
Q

What is the clinical presentation of paracoccidioidomycosis?

A
  • Usually asymptomatic
  • acute, subacute, chronic pneumonia
  • disseminated: lymphadenopaty, organomegaly, and BM involvement
  • chronic mucocutaneous ulcers
  • meningitis
130
Q

How is paracoccidioidomycosis diagnosed and treated?

A

Diagnosis:
Direct microscopy
tissue biopsy
culture

Treatment:
Itraconazoole

Severe: amphotericin B

HIV+ patients: TMP/SMX prophylaxis

Module 3: CPR (10 decks)

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