Respiratory Pathogens: Bacteria and Mycobacteria Flashcards

1
Q

A 30-year-old female presents with high fever, sore throat, lymphadenopathy, splenomegaly and fatigue. Infectious mononucleosis is suspected. Which of the is the most common lab testing method for diagnosing this condition?

A

A test for heterophile antibody, which cross reacts with antigens found on a variety of animal red blood cells

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2
Q

An unvaccinated 60-year-old man develops a sore throat and difficulties in swallowing while on 2 weeks long trip to rural India. Two days after his arrival in Mannitoba, he visited a local hospital. A tough, adherent gray fibrinous exudate in oropharynx along with bilateral cervical lymphadenopathy was noted on physical examination. Which organism is most likely responsible for patient’s symptoms?

A

Diptheria

Gram positive rods with granules

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3
Q

What is an important characterisitic of the streptococcus bacteria?

A

Gram Positive

Catalase NEGATIVE- Used to differentiate from (see panopto 9/10 42min)

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4
Q

What are syndromes that affect the upper respiratory tract?

A
  • Common Cold
  • Pharyngitis
  • Influenza
  • Diphtheria
  • Sinusitis & Otitis media
  • Rhinocerebral mucormycosis
  • Epiglottitis
  • Croup /Laryngitis
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5
Q

What are the syndromes that afect the lower respiratory tract?

A
  • Whooping Cough
  • Bronchitis/ Bronchiolitis
  • Influenza
  • Pneumonias –
    • Typical and Atypical
    • Community, Nosocomial, Occupational, Regional, Opportunistic
  • Pulmonary Tuberculosis
    • Mycobacterium tuberculosis
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6
Q

What are the physical defenses of the respiratory tract?

A
  • Nose: hair, cilia, turbinates and mucus- filter dust and particles; Sneezing
  • Change in direction of the airway
  • Lymphoid tissue: Waldeyer’s tonsillar ring
  • Normal flora
  • Mucus and ciliated cells – coughing
  • Respiratory secretions: lysozyme, sIgA, lactoferrin, mucus
  • Alveolar macrophages
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7
Q

How do pathogens avoid immune defense?

A
  • Bacterial adherence - surface structures
    • (Avoid being caught up in the mucus and expelled out)
  • Extracellular toxins – cytotoxins,
  • Growth in host tissue – intracellular
  • Evasion of host defense mechanism
    • Capsules (avoid phagocytosis), existence in multiple types, production of IgA proteases
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8
Q

What are the gram postive bacterial respiratory pathogens?

A

Streptococcus pyogenes

Streptococcus pneumoniae

Staphylococcus aureus *

Bacillus anthracis

Corynebacterium diphtheriae

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9
Q

What are the gram negative bacterial respiratory pathogens?

A

Legionella pneumophila

Bordetella pertussis

Moraxella catarrhalis

Burkholderia cepacia

Pseudomonas aeruginosa

Acinetobacter baumannii

Klebsiella pneumoniae

Haemophilus influenzae

Francisella tularensis *

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10
Q

What are the bacterial repiratory pathogens (acid fast and non staining)?

A

Mycobacterium tuberculosis (acid fast)

Chlamydophila pneumoniae

Chlamydophila psittaci

Mycoplasma pneumoniae

Coxiella burnetti*

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11
Q

What are the fungal respiratory pathogens?

A
  • Aspergillus spp.
  • Blastomyces dermatitidis
  • Coccidioides immitis
  • Histoplasma capsulatum
  • Rhizopus spp.
  • Mucor spp.
  • Pneumocystis jiroveci
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12
Q

what are the parasitic respiratory pathogens?

A

Ascaris lumbricoides

Strongyloides stercoralis

Hookworms

Paragonimus westermani

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13
Q

Patient presents with sinusitis and otitis media. What pathogens can be at fault?

A

•Streptococcus pneumoniae

  • Haemophilus influenzae
  • Moraxella catarrhalis
  • Pseudomonas aeruginosa
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14
Q

Patient presents with sore throat, dysphagia, fever and swollen lymph glands in the neck in the middle of december. What pathogens could be the cause of these symptoms?

A

Pharyngitis

Adenovirus

Coxsackie virus

Epstein-Barr virus

Herpes Simplex virus

Corynebacterium diphtheriae

Streptococcus pyogenes

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15
Q

A pateint with rhinocerebral mucorycosis could be infected with

A

Rhizopus spp.

Mucor spp.

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16
Q

Patient presents with the symptoms shown. Diagnosis of Diptheria is made. What is the culprit of this disease?

A

Corynebacterium diphtheriae

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17
Q

A baby comes to the clinic with a cough and a high pitched air intake before each cough. What bacterial infection is causing this baby’s symptoms?

A

The baby has whooping cough. Bordetalla pertussis

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18
Q

What is the cause of tuberculosis?

A

mycobacterium tuberculosis

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19
Q

Causes of typical pneumonia

A
  • Streptococcus pneumoniae
  • Staphylococcus aureus
  • Pseudomonas aeruginosa
  • Burkholderia cepacia
  • Klebsiella pneumoniae
  • Acinetobacter baumannii
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20
Q

Causes of atypical pneumonia

A
  • Mycoplasma pneumoniae
  • Chlamydophila pneumoniae
  • Legionella pneumophila
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21
Q

Causes of regional/ occupational/ opportunistic pneumonias

A
  • Regional/Geographic Pneumonias
    • Blastomyces dermatitidis
    • Histoplasma capsulatum
    • Coccidioides immitis
  • Occupational Pneumonias
    • Bacillus anthracis
    • Chlamydophila psittaci
  • Opportunistic Pneumonias
    • Aspergillus spp.
    • Pneumocystis jiroveci
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22
Q

What are the characterisitics of the streptococcus genus?

A

Gram positive cocci

Catalase negative

In chains or pairs

Hemolytic patterns: α, β and γ

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23
Q

Catalase Test

A

Catalase producing organism + H2O2= O2 (bubble)+water

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24
Q

Classification of Streptococcus based on hemolytic properties

A
  • Antigenic grouping – cell wall carbohydrate
    • Lancefield groups: A-H, K-V (Group A is S. pyogens)
  • Serotyping , Group A (GAS)- M protein – M1, M2 etc
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25
Q

Group A Streptococcus (S. pyogens)

general properties

A
  • Gram positive cocci in chains,
  • Catalase negative,
  • beta hemolytic on blood agar plate,
  • bacitracin sensitive,
  • Lancefield group A, PYR +.
  • Group specific carbohydrate (A antigen)
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26
Q

What are the virulance facotrs of S. pyogenes?

A
  • Capsule: Hyaluronic acid - antiphagocytosis
  • M protein: used for serotyping (>150 types)
    • Antiphagocytic: binds to Fc region of IgG and IgA
    • Adhesion factor: binds to collagen, fibrinogen, plasminogen etc.
    • Avoids host immune response –due to antigenic variation
  • F protein: binds to fibronectin
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27
Q

What are the enzymatic virulence factors of S. pyogenes?

A
  • Hemolysins: Streptolysin S and Streptolysin O
    • O is immunogenic (oxygen labile) , S is nonimmunogenic (oxygen stable)
  • Pyrogenic exotoxins: superantigens
  • C5a peptidase: inactivates C5a
  • Streptokinase: lyses blood clots; dissemination
  • Streptodornase (DNase) - dissemination
  • Hyaluronidase: degrades hyaluronic acid
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28
Q

Most Impotant GAS virulance factor

A

M protein

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29
Q

Patient tests positive for strptococcus pyogenes (GAS). What list of diseases could it inflict on the patient?

A
  • Pyogenic infections –include pharyngitis, otitis media, pneumonia, skin and soft tissue infections
  • Toxin mediated – scarlet fever, toxic shock syndrome, fasciitis
  • Rheumatic fever
  • Glomerulonephritis
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30
Q

10 year old presents to you office in Febuary. He hassudden onset of tender enlarged anterior cervial nodes. fever, sore throat for a couple days. Claims to have no cough. What is the diagnoisis?

A

GAS Pharyngitis.

S. Pyogenes

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31
Q

Patient comes with pharyngitis and a rash on the chest and extremities with the presentation below. What is the cause of this presentation?

A

Streptococcal pyrogenic exotoxin A- (Spe A)/ Erythrogenic toxin, which is a super antigen) – produced by lysogenized strains

Scarlet fever- 2nd disease (Streptococcus pyogenes) the bacteria must be infected by a phage

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32
Q

6 yr old boy has a history of pharyngitis 3 weeks ago. Currently presents with fever, migratory polyarthritis, skin rash, subcutaneous nodules. What other symptom do you expect?

A

Patient has Rheumatic Fever. Caused by a type 2 hypersensitivity- immune mediated inflammation. Caused by cross reactivity with M protein.

  • You would expect the patient to have carditis and chorea.

Treat within 3 days of onset for reduced incidence

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33
Q

2 weeks after a skin infection patient presents with edema, hematuria, proteinuria and smoky urine. What is the cause of this patients symptoms?

A

Patient has Acte Post Streptococcal Glomerulonephritis.

Antigen antibody complex deposition on the GBM.

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34
Q

You suspect a patient has a strep pharyngitis. How do you diagnose?

A
  • Throat swab, beta-hemolytic on blood agar, bacitracin sensitive, catalase negative, Gram positive cocci in chains
  • Group A antigen
  • ELISA
    • streptococcal group A cell wall carbohydrate antigen.
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35
Q

What criteria is used to make a rheumatic faver diagnosis?

A

Jones Criteria

Diagnosis based on serological findings (step O (ASO))

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36
Q

How do you diagnose glomerulonephritis?

A

Clinical, history of skin or throat infections, Serology- anti streptolysin O (ASO) and anti-DNase.

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37
Q

how is pharyngitis treated?

A

Penicillin G/or amoxicillin ,

For allergic – Macrolides such as azithro/erythromycin

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38
Q

Treatment of acute glomerulonephritis and rheumatic fever?

A

After onset, antibiotics DONT help

Recovered from rheumatic fever are given monthly dose of benzathine penicillin to prevent further infection

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39
Q

What are the general properties of Streptococcus pneumoniae?

A
  • Gram +ve, encapsulated
  • lancet-shaped (elongated)
  • paired cocci or short chains
  • alpha hemolytic
  • optochin sensitive
  • bile soluble
  • autolyses
  • No Group specific cell wall carbohydrate,
  • >90 capsular serotypes – vaccine antigen
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40
Q

What populations are at risk for a s. pneumoniae inffection?

A
  • Children and elderly
  • Antecedent viral RT infection, such as post- influenza infection
  • Alcoholics, smoking, asthma, chronic pulmonary disease, congestive heart failure (aspiration)
  • Asplenic/splenectomy patients = sepsis/bacteremia
  • Trauma/leakage of CSF to the nose= meningitis
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41
Q

How does strp. pneumoniae colonize cells?

A
  • IgA proteases - disrupt secretory IgA activity
  • Surface protein adhesins
  • Cytotoxin-binds cholesterol in cell-creates pores
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42
Q

How does step. pneumoniae cause tissue infection?

A
  • Teichoic acid and peptidoglycan – activate alternative complem.
  • Pneumolysin: activate classical complem. pathway-inflammation
  • Phosphorylcholine: cell wall binds to receptors (for plasma activiating factor) – bacteria “hide” inside the non-professional phagocytes
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43
Q

What is the main deffence mechanism of s. pneumoniae?

A

Polysaccharide capsule (90 serotypes) –Antiphagocytic

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44
Q

Patient presents with abrupt onset, fever, chills, rigors, cough, chest pain with rusty (blood tinged) sputum. Diagnosis? Pathogen?

A

Lobular Pnaumonia

Pneumoccocal (most common cause of community aquired typical pneumonia)

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45
Q

What are the dieases caused by s/ pneumoniae?

A
  • Meningitis
  • Bacteremia
  • Pneumonia
  • Otitis Media (Sinusitis)- most common
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46
Q

You suspect that cause of a patients pneumonia is S. pneumoniae. How do you confirm the diagnosis?

A
  • Gram stain: Gram positive diplococci, capsule
  • Quellung test: capsular swelling by applying specific antibodies.
  • Culture: Alpha-hemolysis on BAP, Optochin susceptibility
  • Bile solubility: addition of bile salts to culture results in killing of cell – culture becomes less turbid.
  • PCR and/or latex particle agglutination (meningitis)
47
Q

What is a quellung test?

A

A biochemical reaction in which anticapsular antibodies bind to the capsule of a bacterium, resulting in the capsule to swell or become more visible, especially under the microscope.

48
Q

How do we treat S. Pneumoniae?

How can we prevent it?

A
  • Treatment: penicillin/erythromycin. Increasing resistance to penicillin.
    • Alternative drugs- ceftriaxone or vancomycin
  • Prevention: pneumococcal capsular vaccines; two types
    • Adult PPV: 23 valent vaccine (PPV-23): T cell independent
    • Pediatric PCV: 13 valent vaccine (PCV-13), T dependent response
49
Q

What are the characterisits of Heamophilus Influenzae?

A
  • Gram negative coccobacilli (Pleomorphic)
  • Capsulated
  • Fastidious, require growth factors- factor X (hemin) and factor V (NAD) or grow on chocolate agar or near S. aureus on blood agar
  • Catalase and Oxidase positive
  • Several capsular types (a-f). Type b (Hib) most virulent
50
Q

What population is at risk for H. influnzae?

A
  • Anyone
  • unvaccinated children between 2-4 years old- severe disease.
51
Q

What is the most important virulent factor of the H. influenzae?

A
  • Polysaccharide capsule: antiphagocytic
    • Type b capsule is made up of polyribose-ribitol phosphate (PRP) – most invasive diseases are caused by H. influenzae type b (Hib)
52
Q

What are the invasive diseases caused by Hib?

A
  • Meningitis
  • Epiglottitis
  • Bacteremia
53
Q

Patient presents with pink eye. What is the cause of thie disease?

A

H. aegyptius

54
Q

How are strains of H. influenza chategorized?

A
  1. Encapsulated strains were classified on the basis of their distinct capsular antigens. Six types H. influenzae: a, b, c, d, e, and f.
  2. Unencapsulated strains are termed nontypable (NTHi) because they lack capsular serotypes.
55
Q

4 year old child comes to the emergency department with dysphagia, hoarseness, drooling and trouble breathing. On inspiration he has a stidor. Physical exam reveals a cherry red epiglottis and a thumb sign on xray. What do you expect on cultures?

A

This child has a invasive epiglottitis caused by Hib.

  • Chocolate agar or blood agar with S. aureus streak.
  • Antigen Detection: latex agglutination- Rapid PRP capsular antigen for H. influenzae type b only
56
Q

What treatment do you give to a suspected case of epiglottitis?

A
  • Hospitalized immediately
  • Antibiotic treatment :
    • severe cases – broad-spectrum cephalosporin
    • mild cases – amoxicillin, doxycycline
57
Q

How is H. influenzae prevented?

A
  • Immunoprophylaxis: Hib (PRP) Vaccine directed to type b capsular polysaccharide; conjugated to diphtheria toxoid or tetanus toxoid
  • Chemoprophylaxis : rifampin in high risk
58
Q

A 12-year-old girl presents with ear pain and fever. Physical exam reveals perforated ear drum that is exuding a small amount of pus. Gram stain of the pus revealed Gram negative coccobacilli. There was no growth on blood agar but small grey colonies appeared on chocolate agar. Which microbes is the most likely pathogen?

A

Haemophilus influenzae

59
Q

An unvaccinated 60-year-old man develops a sore throat and difficulties in swallowing while on 2 weeks long trip to rural India. Two days after his arrival in Mannitoba, he visited a local hospital. A tough, adherent gray fibrinous exudate in oropharynx along with bilateral cervical lymphadenopathy was noted on physical examination. Which organism is most likely responsible for patient’s symptoms?

  1. Gram positive cocci in chains
  2. Gram positive cocci in clusters
  3. Gram positive lancet shaped cocci
  4. Gram positive rods with granules
  5. Gram negative coccobacilli
A

Patient has diphtheria.

D. Corynebacterium diphtheriae

60
Q

What are the caracteristics og Corynebacterium Diphtheriae?

A
  • Pleomorphic
  • Gram positive rods
  • clubbed ends
  • coryneform (club shaped
  • V and L shaped pairs
  • Formation of granules (volutin)
  • beaded appearance
  • metachromatism
61
Q

When does C. diptheriae become toxic to humans

A

When the bacteria is infected a phage, aquire a tox gene and become lysogenized.

62
Q

What populations are at risk for C. diptheriae?

A
  • Unvaccinated (incidence ↓sed with vaccine)
  • crowded condition
  • mostly children
63
Q

How does iron affect the toxicity of C. diphtheriae?

A
  • Low levels of iron: the protein de-represses toxin gene - toxin production
  • High levels of iron: the protein is activated and represses the gene – no toxin production
64
Q

What is the effect of the diphtheria toxin?

A
  1. Binds to heparin-binding epidermal growth factor (HB-EGF)
  2. Inhibits protein synthesis via ADP ribosylation/ inactivation of EF-2
  3. Cell dies
65
Q

If the diphtheria toxin travels to ther organs what are sever complications tht can arise?

A
  • Myocarditis (arrythmia and circ. collapse)
  • Nerve weakness/ paralysis (cranial nerves)
66
Q

What diagnostic test are used for C. diphtheriae?

A
  • Culture–
    • Blood agar (Enriched)- small hemolysis
    • Cysteine- tellurite blood agar (gray black colony)
    • Loeffer’s serum plate (granule formation)
  • Toxin testing:
    • Elek’s test –principle of Ouchterlony
67
Q

How do we treat diptheria?

How do we prevent it?

A
  • Treatment
    • Early administration of the diphtheria antitoxin (passive immunity)
    • Penicillin or erythromycin
    • Respiratory support
  • Prevention
    • Vaccine (DPT; Now 4 combinations-DTaP, DT, Tdap, Td
68
Q

What are the caracteristics of Bordetella Pertussis?

A
  • Gram negative coccobacillus
  • strict aerobic
  • Capsulated
  • Non motile
  • Requires enriched culture media, Bordet-Gengou media
  • Resistant to penicillin
69
Q

What is the pathogenesis of B. Pertussis?

A

This pathogen adheres and multiplies rapidly on the epithelial surface of the trachea & bronchi

  • increased respiratory secretions; and
  • interferes with ciliary action (clearance).
70
Q

What are the characterisics of Bordetella Pertussis?

A
  • Gram negative coccobacillus: strict aerobic
  • Capsulated
  • Non motile
  • Requires enriched culture media, Bordet-Gengou media (potato-blood-glycerol agar with 20-30% blood) , Resistant to penicillin – so penicillin is added in the media to make media selective
71
Q

How does B. pertussis adhere to the bronchi?

A
  • Conatins Adhesins
    • Filamentous hemagglutinin (FHA) and Pertactin
  • Bind to integrins on ciliated cells
  • Bind to CR3 (complement receptor) on macrophages and induce phagocytosis without initiating oxidative killing
72
Q

What are the txoins of B. pertussis?

A
  • 1. Pertussis toxin (PTx) – AB type toxin
    • ADP ribosylation of Gi protein; increased cAMP level
    • Interferes chemokine production
    • Inhibits neutrophil chemotaxis
  • 2. Tracheal Cytotoxin (Peptidoglycan subunit)
    • Cilliostasis. Inhibit regeneration
    • Characteristic cough
  • 3. Adenylate cyclase toxin:
    • Activated by calmodulin, ATP to cAMP
    • Effect same as above
73
Q

What are additional complicaitons of B. Pertussis?

A
  • Increased histamine sensitivity: allergic like reaction
  • Sensitization of beta-islet cells: Hyperinsulinemia-hypoglycemia
74
Q

When is whooping cough the most contagious?

A

The bacterial culture increases during week 1 and 2- Catarrhal stage

75
Q

What are the stages of whooping cough?

A
  1. Catarrhal (lasts 1-2 weeks): common cold: highly contagious at this stage
  2. Paroxysmal (2-4 weeks): destruction of ciliated epithelium; impairment of mucous clearing; spasmodic cough with whoops. leukocytosis
  3. Convalescent: secondary complications due to lack of oxygen supply: Pneumonia, seizures, encephalopathy
76
Q

What is a nasal swab for B. pertussis done with?

A

Calcium alginate swab

77
Q

What is the cultre for B. Pertussis?

A
  • Standard: Bordet-Gengou, Charcoal-cephalexin blood agar OR Regan-Lowe
    • Nicotinic support growth
    • charcoal, starch or blood adsorb fatty acids/toxins
  • PCR
  • ELISA
78
Q

What is the treatment for B. pertussis?

A
  • Macrolides: Early stage: erythromycin azithromycin
  • Supportive – for late stage:
    • suctioning, rehydration, oxygenation, anti-inflammatory agents
79
Q

Prevention of B. Pertussis

A
  • Vaccine: 2 types (Whole cell killed and acellular)
  • DPT vaccine (diphtheria, pertussis, tetanus): whole cell inactivated- not used in USA
  • DTaP vaccine: for children (2months to 6 Years, 5 doses)
    • Multivalent acellular vaccine-effective; less side effects
    • Immunogen is the pertussis toxoid
  • Tdap: as a booster
  • Antibiotic prophylaxis: erythromycin prophylaxis in close contact
80
Q

What are side effects of using whole cell killed vaccine for B. Pertussis?

A
  • produced convulsions and encephalopathy in few vaccinated people
  • Acellular vaccine has fewer side effects than the killed vaccine but has shorter duration of immunity.
81
Q

What are the characterisitics of Moraxella Catarrhalis?

A
  • Gram negative diplococci (bean shaped)
  • family Neisseriaceae
  • oxidase positive
  • Does not ferment glucose, maltose and sucrose.
82
Q

What agar for m.cararrhlis grow on?

A

Blood agar

83
Q

What is the treatment of M. catarhalis?

Prevention?

A
  • 95% of isolates in the US are beta-lactamase positive and penicillin resistant
  • Amoxycillin+clavulanate (Augmentin), 2nd or 3rd generation oral cephalosporins, TMP/SMX
84
Q

What are the clinical symptoms of moracella Catarrhalis?

A
  • otitis media (3rd most common cause)
  • sinusitis in children
  • bronchitis and pneumonia in elderly.
85
Q

How are mycobacterium classified?

A

Runyon classification

  • Rate of growth:
    • Fast growers (˂7days)
    • Slow growers (several weeks)
  • Production of yellow pigment
    • Scotochromogens: Pigment in the dark
    • Photochromogens: Pigment only after exposure to light
    • Nonchromogens : no color or slight tan color
86
Q

Which mycobacteria cause pulmunary infections?

A
  • M. tuberculosis – causes TB, strictly human pathogen
  • M. bovis – from animals, transmitted via raw milk, TB
  • M. avium complex (MAC) – TB like disease, mostly in HIV patients, found in soil and water (atypical)
  • M. kansasii –TB like disease mostly in HIV patients, found in soil and water (atypical)
87
Q

Which mycobacteria cause skin infections?

A
  • M. leprae – causes leprosy, strictly human pathogen
  • M. marinum – found in water, causes skin granuloma “ fish tank granuloma”, swimming pool granuloma” (atypical)
  • M. ulcerans – found in soil/water, causes skin infection known as buruli ulcer, tropical disease (atypical)
88
Q

What are the general characterisitics of M. tuberculosis?

A
  • Acid fast bacilli,
  • obligate aerobe
  • non spore forming bacteria
  • High guanine + cytosine (G+C) contents in DNA
  • Weakly Gram positive
  • Cell wall rich in complex lipids
  • Slow grower
  • Produces niacin
89
Q

Why are some species of mycobacteria clasifed as atypical?

A

They differ in certain respects from the prototype, M. tuberculosis. The atypical mycobacteria are sometimes called Mycobacteria Other Than Tuberculosis (MOTTS)

90
Q

What is the structure of the mycobacterium cell wall?

A

The peptidoglycan layer is linked to arabinogalactan which is then linked to high-molecular weight mycolic acids. Mycolic acids make up 50% of the dry weight of the mycobacterium cell envelope.

91
Q

The high concentration of lipids on the mycobacterium cell wall are benefit to the pathogen in which ways?

A
  • Impermeability to stains and dyes
  • Resistance to many antibiotics
  • Resistance to killing by acidic and alkaline compounds
  • Resistance to complement attack
  • Resistance to lethal oxidations; and survival inside of macrophages
92
Q

What is the cord factor?

A
  • (Trehalose dimycolate)
  • Part of the surface lipid: present only in virulent strains
  • Inhibits leucocyte migration; disrupts mitochondrial respiration and oxidative phosphorylation
  • serpentine appearance in culture
93
Q

What populations are at risk for M. tuberculosis?

A
  • Economically disadvantaged people-
  • homeless,
  • malnourished,
  • compromised immune system (eg. HIV),
  • crowded conditions,
  • drug or alcohol abusers

1/3 of population is infected only immunodeficient people become sick

94
Q

What is the virulence of M. tuberculosis?

A
  • Does not produce exotoxin & endotoxin, has no capsule
  • Preventing formation of phagolysosome (fusion of phagosome and lysosomes):
    • exported repetitive protein (ERP);
    • sulfatides and sulpholipids that hydrolyze into sulfuric acid
  • preventing oxidative killing
95
Q

How does the immune system combact M. tuberculosis?

A
  1. The bacteria resist intracellular killing inside macrophages
  2. The infected macrophages secrete IL-12 and TNFα which recruit inflammatory cells
  3. Infected macrophages present the antigen to T lymphocytes
  4. Differentiation of Th to Th1 occurs
  5. Th1 secrete INFγ which activates the macrophages to kill the bacteria
96
Q

What will be the histological aperance of the lung in tuberculosis?

A

Ghon Complex- Granuloma formation

  • Central Caseous necrosis
  • Multinucleated giant cell
  • Epitheloid Macrophages
97
Q

What is the pathologic changes of M. Tuberculosis?

A
  • After macrophages are activated.
  • Granulomatous lesions/Ghon focus: Located around alveoli in the lung. Bacteria may remain viable for long time
  • Ghon complex: granuloma with central caseous necrosis (i.e Ghon focus + LN involvement)
  • Tubercle: a granuloma surrounded by fibrous tissue
98
Q

What are the stages of tuberculosis infection?

A
  • No disease: Arrested within the granuloma. Bacteria eliminated
  • Primary infection: bacterial replication is not arrested
  • Miliary tuberculosis: tubercle lesion may rupture- spread to several organs, extra-pulmonary tuberculosis
  • Latent infection: bacteria remain viable in the granuloma
  • Secondary infection: Impairment of the immune system reactivation of TB from a granuloma and spread
99
Q

What is the most common site of extrapulmonary tuberculosis?

A

Lymphadenitis- in the neck

Scrofula is mycobacterial cervical lymphadenitis

100
Q

What is Pott’s Disease?

A

A form of tuberculosis that occurs outside the lungs in the vertebrae. Tuberculosis can affect several tissues outside of the lungs including the spine, a kind of tuberculous arthritis of the intervertebral joints.

101
Q

Patient comes in with bloody sputum, fever, chills, night sweats, and weight loss. What is the diagnosis?

A

Primary TB- lower part of the lung

102
Q

What are the clinical symptoms of the varient stages of TB?

A
  • Latent tuberculosis: no clinical symptoms, bacteria remain alive inside granuloma
  • Reactivation tuberculosis: upper part of lung, similar symptoms as primary
  • Miliary (multiple foci) : disseminated disease of many tissues
103
Q

How is TB diagnosed?

A
  • X-ray: used in conjunction with PPD – looking for tubercles, Ghon complexes, cavitary lesions
  • Staining and Microscopy (Sputum/other specimens) : Acid fast staining
  • Culture – isolation of organisms in Lowenstein-Jensen (LJ) medium or Middlebrook 7H10 (may take up 2 to 8 weeks for results)- Gold standard
104
Q

What are the risk guidelines for a PPD test?

A
  • 5 mm or more
    • HIV-positive person, recent contacts, abnormal CXR
  • 10 mm or more
    • Recent migrants prevalence regions
    • Residents of crowded institutions
    • Health care workers
    • Persons with other medical issues.
  • 15 mm or more
    • No known risk factors
105
Q

Patient presents with bloody cough and the following xray. What is the arrow pointing to?

A

Cavity in patient’s right upper lobe. Left lung is normal

106
Q

What method can be used to diagnose M. Tuberculosis under microscope?

A
  • Auramine rhodamine staining
    • Stained with auramine –rhodamine and viewed with fluorescence microscopy (acid fast bacilli appear as glowing yellow rods)
  • Ziehl-Neelsen stain (Acid fast staining)
107
Q

What antigens will be found in the blood of patients with TB?

A

Two M.tb specific antigens : ESAT-6 or CFP-10

If the patients were infected, their Th1 specific to MTB would be primed and produce IFN-γ (ELISA)

108
Q

How is TB treated?

A

Multi-drug for several months - 6 to 9 months

  • Isoniazid (H)
  • Rifampin (R)
  • Pyrazinamide (Z)
  • Ethambutol (E)
109
Q

How are resistant strains of TB treated?

A
  • MDR-TB: multi drug resistant—to isoniazid and rifampin
  • XDR-TB: extensively drug resistant- to isoniazid and rifampin, plus any fluoroquinolone and at least one of three injectable second-line drugs (i.e., amikacin, kanamycin, or capreomycin); not easy to treat
110
Q

What is the TB vaccine?

A

BCG vaccine (Bacille Calmette-Guerin), a live attenuated bovine strain (i.e., M. bovis)

111
Q

In what cases would a TB vaccine be given in the US?

A
  • children with close contact of TB patients; and
  • Military personnel
112
Q

A 45-year-old homeless man presents to the emergency department with fever and night sweats, coughing up blood. Acid fast bacilli are identified in his sputum.

Regarding pathogenesis of the above disease, which of the following events must have occurred first after the acquired the infection?

  1. Secretion of IL-12 and TNFα by macrophages
  2. Activation of Th1 cell
  3. Inhibition of phagosome-lysosome fusion in Macrophages
  4. Formation of Langhan’s giant cell
  5. Formation of Ghon complex
A

Inhibition of phagosome-lysosome fusion in Macrophages

113
Q

A 45-year-old homeless man presents to the emergency department with fever and night sweats, coughing up blood. Acid fast bacilli are identified in his sputum.

Which of the following virulence factors allows the causal agent to inhibit the phagosome-lysome fusion to survive intracellularly?

  1. Cord factor
  2. Calcium dipicolonate
  3. Peptidoglycan
  4. Sulfatides
  5. Tuberculin
A

Sulfatides

114
Q

Patient presents with trouble swalloing, drooling and a change in voice. Her condition is brought on by a virus. What is the diagnosis? bacteria?

A
  • Epiglottitis

Haemophilus influenzae