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
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
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)
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
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
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
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
8
Q
What are the gram postive bacterial respiratory pathogens?
A
Streptococcus pyogenes
Streptococcus pneumoniae
Staphylococcus aureus *
Bacillus anthracis
Corynebacterium diphtheriae
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 *
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*
11
Q
What are the fungal respiratory pathogens?
A
- Aspergillus spp.
- Blastomyces dermatitidis
- Coccidioides immitis
- Histoplasma capsulatum
- Rhizopus spp.
- Mucor spp.
- Pneumocystis jiroveci
12
Q
what are the parasitic respiratory pathogens?
A
Ascaris lumbricoides
Strongyloides stercoralis
Hookworms
Paragonimus westermani
13
Q
Patient presents with sinusitis and otitis media. What pathogens can be at fault?
A
•Streptococcus pneumoniae
- Haemophilus influenzae
- Moraxella catarrhalis
- Pseudomonas aeruginosa
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
15
Q
A pateint with rhinocerebral mucorycosis could be infected with
A
Rhizopus spp.
Mucor spp.
16
Q
Patient presents with the symptoms shown. Diagnosis of Diptheria is made. What is the culprit of this disease?
A
Corynebacterium diphtheriae
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
18
Q
What is the cause of tuberculosis?
A
mycobacterium tuberculosis
19
Q
Causes of typical pneumonia
A
- Streptococcus pneumoniae
- Staphylococcus aureus
- Pseudomonas aeruginosa
- Burkholderia cepacia
- Klebsiella pneumoniae
- Acinetobacter baumannii
20
Q
Causes of atypical pneumonia
A
- Mycoplasma pneumoniae
- Chlamydophila pneumoniae
- Legionella pneumophila
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
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
23
Q
Catalase Test
A
Catalase producing organism + H2O2= O2 (bubble)+water
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
25
Group A Streptococcus (S. pyogens)
general properties
* Gram positive cocci in chains,
* Catalase negative,
* beta hemolytic on blood agar plate,
* **bacitracin sensitive,**
* **Lancefield group A, PYR +.**
* Group specific carbohydrate (A antigen)
26
What are the virulance facotrs of S. pyogenes?
* 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
27
What are the enzymatic virulence factors of S. pyogenes?
* _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
28
Most Impotant GAS virulance factor
M protein
29
Patient tests positive for strptococcus pyogenes (GAS). What list of diseases could it inflict on the patient?
* Pyogenic infections –include **pharyngitis, otitis media, pneumonia**, skin and soft tissue infections
* Toxin mediated – **scarlet fever,** toxic shock syndrome, fasciitis
* **Rheumatic fever**
* **Glomerulonephritis**
30
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?
GAS Pharyngitis.
S. Pyogenes
31
Patient comes with pharyngitis and a rash on the chest and extremities with the presentation below. What is the cause of this presentation?
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
32
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?
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
33
2 weeks after a skin infection patient presents with edema, hematuria, proteinuria and smoky urine. What is the cause of this patients symptoms?
Patient has Acte Post Streptococcal Glomerulonephritis.
Antigen antibody complex deposition on the GBM.
34
You suspect a patient has a strep pharyngitis. How do you diagnose?
* **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.
35
What criteria is used to make a rheumatic faver diagnosis?
**Jones Criteria**
## Footnote
Diagnosis based on serological findings **(step O (ASO))**
36
How do you diagnose glomerulonephritis?
Clinical, history of skin or throat infections, **Serology- anti streptolysin O (ASO) and anti-DNase.**
37
how is pharyngitis treated?
Penicillin G/or amoxicillin ,
For allergic – Macrolides such as azithro/erythromycin
38
Treatment of acute glomerulonephritis and rheumatic fever?
After onset, antibiotics DONT help
Recovered from rheumatic fever are given monthly dose of benzathine penicillin to prevent further infection
39
What are the general properties of Streptococcus pneumoniae?
* 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
40
What populations are at risk for a s. pneumoniae inffection?
* 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_
41
How does strp. pneumoniae colonize cells?
* IgA proteases - disrupt secretory IgA activity
* Surface protein adhesins
* Cytotoxin-binds cholesterol in cell-creates pores
42
How does step. pneumoniae cause tissue infection?
* 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
43
What is the main deffence mechanism of s. pneumoniae?
Polysaccharide capsule (90 serotypes) –Antiphagocytic
44
Patient presents with abrupt onset, fever, chills, rigors, cough, chest pain with rusty (blood tinged) sputum. Diagnosis? Pathogen?
Lobular Pnaumonia
Pneumoccocal (most common cause of community aquired typical pneumonia)
45
What are the dieases caused by s/ pneumoniae?
* Meningitis
* Bacteremia
* Pneumonia
* Otitis Media (Sinusitis)- most common
46
You suspect that cause of a patients pneumonia is S. pneumoniae. How do you confirm the diagnosis?
* **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
What is a quellung test?
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
How do we treat S. Pneumoniae?
How can we prevent it?
* **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
What are the characterisits of Heamophilus Influenzae?
* 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
What population is at risk for H. influnzae?
* Anyone
* unvaccinated children between 2-4 years old- severe disease.
51
What is the most important virulent factor of the H. influenzae?
* 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
What are the invasive diseases caused by Hib?
* Meningitis
* Epiglottitis
* Bacteremia
53
Patient presents with pink eye. What is the cause of thie disease?
H. aegyptius
54
How are strains of H. influenza chategorized?
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
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?
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
What treatment do you give to a suspected case of epiglottitis?
* Hospitalized immediately
* Antibiotic treatment :
* severe cases – **broad-spectrum cephalosporin**
* mild cases – amoxicillin, doxycycline
57
How is H. influenzae prevented?
* Immunoprophylaxis: Hib (PRP) Vaccine directed to type b capsular polysaccharide; _conjugated to diphtheria toxoid or tetanus toxoid_
* Chemoprophylaxis : rifampin in high risk
58
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?
Haemophilus influenzae
59
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
Patient has diphtheria.
D. Corynebacterium diphtheriae
60
What are the caracteristics og Corynebacterium Diphtheriae?
* Pleomorphic
* Gram positive rods
* clubbed ends
* coryneform (club shaped
* V and L shaped pairs
* Formation of granules (volutin)
* beaded appearance
* metachromatism
61
When does C. diptheriae become toxic to humans
When the bacteria is infected a phage, aquire a tox gene and become lysogenized.
62
What populations are at risk for C. diptheriae?
* Unvaccinated (incidence ↓sed with vaccine)
* crowded condition
* mostly children
63
How does iron affect the toxicity of C. diphtheriae?
* 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
What is the effect of the diphtheria toxin?
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
If the diphtheria toxin travels to ther organs what are sever complications tht can arise?
* Myocarditis (arrythmia and circ. collapse)
* Nerve weakness/ paralysis (cranial nerves)
66
What diagnostic test are used for C. diphtheriae?
* 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
How do we treat diptheria?
How do we prevent it?
* 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
What are the caracteristics of Bordetella Pertussis?
* Gram negative coccobacillus
* strict aerobic
* Capsulated
* Non motile
* Requires **enriched** culture media, **Bordet-Gengou media**
* Resistant to penicillin
69
What is the pathogenesis of B. Pertussis?
This pathogen adheres and multiplies rapidly on the epithelial surface of the trachea & bronchi
* increased respiratory secretions; and
* interferes with ciliary action (clearance).
70
What are the characterisics of Bordetella Pertussis?
* 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
How does B. pertussis adhere to the bronchi?
* 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
What are the txoins of B. pertussis?
* **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
What are additional complicaitons of B. Pertussis?
* Increased histamine sensitivity: allergic like reaction
* Sensitization of beta-islet cells: Hyperinsulinemia-hypoglycemia
74
When is whooping cough the most contagious?
The bacterial culture increases during week 1 and 2- Catarrhal stage
75
What are the stages of whooping cough?
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
What is a nasal swab for B. pertussis done with?
Calcium alginate swab
77
What is the cultre for B. Pertussis?
* Standard: **Bordet-Gengou, Charcoal-cephalexin blood agar OR Regan-Lowe**
* Nicotinic support growth
* charcoal, starch or blood adsorb fatty acids/toxins
* PCR
* ELISA
78
What is the treatment for B. pertussis?
* Macrolides: Early stage: erythromycin azithromycin
* Supportive – for late stage:
* suctioning, rehydration, oxygenation, anti-inflammatory agents
79
Prevention of B. Pertussis
* 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
What are side effects of using whole cell killed vaccine for B. Pertussis?
* 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
What are the characterisitics of Moraxella Catarrhalis?
* Gram negative diplococci (bean shaped)
* family Neisseriaceae
* oxidase positive
* Does not ferment glucose, maltose and sucrose.
82
What agar for m.cararrhlis grow on?
Blood agar
83
What is the treatment of M. catarhalis?
Prevention?
* 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
What are the clinical symptoms of moracella Catarrhalis?
* otitis media (3rd most common cause)
* sinusitis in children
* bronchitis and pneumonia in elderly.
85
How are mycobacterium classified?
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
Which mycobacteria cause pulmunary infections?
* **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
Which mycobacteria cause skin infections?
* **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
What are the general characterisitics of M. tuberculosis?
* **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
Why are some species of mycobacteria clasifed as atypical?
They differ in certain respects from the prototype, M. tuberculosis. The atypical mycobacteria are sometimes called Mycobacteria Other Than Tuberculosis (MOTTS)
90
What is the structure of the mycobacterium cell wall?
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
The high concentration of lipids on the mycobacterium cell wall are benefit to the pathogen in which ways?
* 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
What is the cord factor?
* (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
What populations are at risk for M. tuberculosis?
* 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
What is the virulence of M. tuberculosis?
* 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
How does the immune system combact M. tuberculosis?
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
What will be the histological aperance of the lung in tuberculosis?
Ghon Complex- Granuloma formation
* Central Caseous necrosis
* Multinucleated giant cell
* Epitheloid Macrophages
97
What is the pathologic changes of M. Tuberculosis?
* 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
What are the stages of tuberculosis infection?
* **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
What is the most common site of extrapulmonary tuberculosis?
Lymphadenitis- in the neck
Scrofula is mycobacterial cervical lymphadenitis
100
What is Pott's Disease?
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
Patient comes in with bloody sputum, fever, chills, night sweats, and weight loss. What is the diagnosis?
Primary TB- lower part of the lung
102
What are the clinical symptoms of the varient stages of TB?
* 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
How is TB diagnosed?
* 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
What are the risk guidelines for a PPD test?
* **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
Patient presents with bloody cough and the following xray. What is the arrow pointing to?
Cavity in patient’s right upper lobe. Left lung is normal
106
What method can be used to diagnose M. Tuberculosis under microscope?
* 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
What antigens will be found in the blood of patients with TB?
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
How is TB treated?
Multi-drug for several months - 6 to 9 months
* Isoniazid (H)
* Rifampin (R)
* Pyrazinamide (Z)
* Ethambutol (E)
109
How are resistant strains of TB treated?
* **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
What is the TB vaccine?
BCG vaccine (Bacille Calmette-Guerin), a live attenuated bovine strain (i.e., M. bovis)
111
In what cases would a TB vaccine be given in the US?
* children with close contact of TB patients; and
* Military personnel
112
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
Inhibition of phagosome-lysosome fusion in Macrophages
113
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
Sulfatides
114
Patient presents with trouble swalloing, drooling and a change in voice. Her condition is brought on by a virus. What is the diagnosis? bacteria?
* Epiglottitis
Haemophilus influenzae
