W2P2 Flashcards

1
Q

Meningitis definition

A

Inflammatory disease of the leptomeninges, the tissues surrounding the brain and spinal cord

Meninges include: dura mater, arachnoid, pia mater

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2
Q

What are the categories of Meningitis

A
Bacterial
Viral
Fungal
Mycobacterial
Parasitic

all types can cause meningitis, but we’re going to be focusing on the BACTERIAL AND VIRAL meningitis

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3
Q

Modes of Acquiring Bacterial Meningitis

A
  1. Community-acquired

2. Healthcare-associated-Post neurosurgical

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4
Q

What are the Pathogens that cause Bacterial Meningitis in Ages less than 1 month

A

Think of GEL

Group B streptococcus [strep agalactiae]
Escherichia Coli
Listeria Monocytogenes

Less than 1 month olds get infections with MATERNAL stool organisms. The GEL pathogens are all ones that live in the stool

  • this will determine which antibiotic you choose.
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5
Q

What are the Pathogens that cause Bacterial Meningitis in Ages 1- 23 months and 2-50 years old

A

Community acquired ones like:

steptococcus pneumoniae
Neisseria Meningitis

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6
Q

What are the Pathogens that cause Bacterial Meningitis in Ages greater than 50 years

A

S. pneumoniae
N. meningitidis
L. monocytogenes
Aerobic Gram negative bacilli

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7
Q

Neisseria Meningitis

  • mortality
  • Which serogroups do we have vaccines for?
  • Which serogroup is the most common in NA?
A

Has a high mortality: 10-20%
Has many different serogroups, know that we have vaccines for: A,B,C W-135 and Y)
- Serogroup B is most common
- Monovalent vaccine against serogroup B now available.

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8
Q

Risk factors for getting Neisseria Meningitis

  • Mode of transmission
A

Risk Factors:

  • Terminal complement deficiencies
  • Functional or anatomic asplenia (e.g. sickle cell)
  • Household exposure to an infected person

Transmission- Droplets respiratory secretions/saliva
Nasal carriage – up to 10% of healthy individuals

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9
Q

Which type of bacterial meningitis has the highest mortality

A

Listeria Monocytogenes

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10
Q

Streptococcus Pneumoniae Meningitis

  • Route of Transmission
  • Risk factors
A

high mortality
- Droplets

Risk Factors
Functional or anatomic asplenia (e.g. sickle cell)
Multiple myeloma
Hypogammaglobulinemia
Alcoholism
Chronic liver disease
Chronic kidney disease
Malignancy
Diabetes mellitus
Cochlear implants
CSF leak (e.g. from basilar skull fracture)
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11
Q

People with functional or anatomic asplenia are at higher risk of

A

getting infected by encapsulated organisms

i.s. strep pneumoniae and neisseria

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12
Q

Haemophilus influenzae Meningitis

  • prelavence
  • risk group
  • Mode of transmission
A

With vaccination since 1998, meningitis due to H. influenzae type b is rare
Accounts for less than 5% of meningitis cases

Occurs primarily in unimmunized or partially immunized children

Transmission-Droplets

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13
Q

Listeria monocytogenes Meningitis

- mode of transmission (examples*)

A

Not as common
we carry it in our stool
however this one is NOT associated with droplet transmission it is FECAL-ORAL transmission

Accounts for approximately 2-8% of meningitis cases
Acquisition-contaminated (stool) foods
- Coleslaw
- Raw vegetables
- Milk and cheese (especially unpasteurized)
- Processed meats

most people have been infected with this and it goes away on its own EXCEPT for people at risk (pregnant women and those at the extremes of ages)

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14
Q

Risk factors for getting Listeria monocytogenes Meningitis

A
Risk Factors:
Neonates (up to 10% of cases)
Adults  60 years
Alcoholics
Malignancy
Immunosuppressed (e.g. transplants, corticosteroids)
Diabetes mellitus
Liver disease
Chronic renal disease
Conditions with iron overload 
Pregnant women (25% of all cases of listeriosis)
Mortality 15-30%
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15
Q

Streptococcus agalactiae Meningitis

A

Also known as Group B Streptococcus

Most common cause of meningitis in neonates
Mortality rate-7% to 27%

Isolated from vaginal or rectal cultures of 15% to 35% of asymptomatic pregnant women

Screening of pregnant women at 35-37 weeks gestation

GBS positive pregnant women receive intrapartum antibiotics to decrease mother to child transmission

Screening and intrapartum abx: 3-fold decrease in transmission

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16
Q

Bacterial Meningitis
Healthcare-associated pathogens

A

Aerobic gram negative bacilli, including Pseudomonas aeruginosa - 40% of cases

Staphylococcus

  • Coagulase negative
  • S. aureus

Propionibacterium acnes (Teenagers, acne prone skin)

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17
Q

What are the three viral groups that give you viral meningitis

A
  1. Herpes simplex (mostly HSV-2)
    - most deadly
  2. Enteroviruses
    - most COMMON: 85-95% of viral meningitis
    - Echoviruses and coxsackieviruses
    - Person to person transmission
    - Seasonality: summer and fall
3. Arboviruses (arthropod-borne viruses)
Transmitted by arthropods (mosquitoes, ticks)
West Nile
St. Louis 
Eastern Equine
Western Equine
California
  • all these can cause Enchephalitis
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18
Q

Parameningeal foci of infection

A

Brain abscess, subdural empyema, epidural abscess, sinusitis, mastoiditis, etc..

^ these things can rupture INTO the CNS, this is a form of SECONDARY meningitis.

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19
Q

Meningitis Clinical Manifestations in Children

A
Non-specific in infants
Fever
Poor feeding
Vomiting
Lethargy
Irritability
Bulging fontanelle (late finding)
Seizures
Older children
Fever
Vomiting
Headache with photophobia
Neck stiffness
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20
Q

Meningitis Clinical Manifestations in Adults

A
Top THREE are most common* 
Fever
Headache
Neck stiffness (Meningismus)
Altered mental status 
Brudzinski’s sign
Kernig’s sign
Jolt accentuation
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21
Q

Brudzinski’s sign

A

B for Brain

Also known as Nape-of-the-neck sign
Passive flexion of the neck results in flexion of the hips and knees
Sensitivity: 5%
Specificity: 95%

  • sensitivity is low, so just because it you get a negative sign, does not mean you can rule it out
    however specificity is high, so positive sign highly likely to be meningitis

positive sign: stretching the neck will cause them to RESIST you from lifting their neck

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22
Q

Kernig’s sign

A

K for Knee

Patient supine, with the thigh flexed on the abdomen and the knee flexed

Leg is then passively extended

In the presence of meningeal inflammation, the patient resists leg extension.

Sensitivity: 5%
Specificity: 95%

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23
Q

Jolt test

A

Jolt accentuation
Patient is asked to quickly move their head from side to side in horizontal plane
If meningeal irritation is present: headache gets worse
Sensitivity: 21-64%
Specificity: 43-82%

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24
Q

Meningitis with RASH suggests which bacterial pathogen

A

Rash suggests 
N. meningitidis -seen in 75% of cases

Rash can also be seen in pneumococcal and enteroviral meningitis

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25
Q

Meningitis with Cranial nerve findings and difficulty breathing is suggestive of

A


L. monocytogenes (rhombencephalitis)

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26
Q

Clinical Management of Meningitis

A
ABCs
Level of consciousness-Possible intubation
Circulation-blood pressure
Blood cultures
Lumbar puncture (LP)
Empiric antibiotics

CT scan (before LP) should be

  • done in the following:
  • Immunocompromised
  • History of CNS disease
  • Focal neurologic deficit
  • New-onset seizure
  • Papilledema
  • Abnormal level of consciousness
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27
Q

Bacterial Meningitis vs Viral Meningitis

A

Bacterial: HIGH PRESSURE
HIGHER cell count [WBC and neutrophils] (viral is high too but bacterial is like 5 times higher)
and thus also comes with HIGH INTRACRANIAL pressure, so you’ll need an Lumbar puncture to relieve the pressure

AND characteristic in BACTERIAL
you’ll see CNS/serum glucose less than 60%

in viral

  • less WBC, less neutrophils
  • protein is whatever
  • glucose is normal
  • gram stain is NEG cause it’s a virus
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28
Q

gram neg dipplococci Meningitis

A

Neisseria meningitis

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29
Q

Gram Negative coccobacilli Meningitis

A

Haemophilus Influenzae

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30
Q

Gram Positive cocci in pairs (diplococci)

A

Streptococcus pneumoniae

Group B streptococcus

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31
Q

Gram positive Rods in Meningitis

A

Listeria Monocytogenes

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32
Q

Empiric Treatment for Neonatals

- What are the usual organisms

A

Group B streptococcus
Gram negative enteric rods
Listeria monocytogenes

ABs:
Ampicillin IV + Cefotaxime IV

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33
Q

Empiric Treatment for Infant (1-3 months)

- What are the usual organisms

A

Group B streptococcus
Gram negative enteric rods
Listeria monocytogenes
Streptococcus pneumoniae

Treatment:
Ampicillin IV + Vancomycin IV
+
Cefotaxime or Ceftriaxone IV

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34
Q

Empiric Treatment for Infant Pediatric (> 3 months)
and adult up to 50 years
- Usual Organisms

A

Streptococcus pneumoniae
Neisseria meningitidis
Haemophilus influenzae (type B)

EMPIRIC antibiotics
Cefotaxime or Ceftriaxone IV
+
Vancomycin IV

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35
Q

Empiric Therapy for Meningitis Adult (>50 years) and
immunocompromised
- Usual organisms

A

Streptococcus pneumoniae
Neisseria meningitidis
Listeria monocytogenes

ABs:
Ampicillin IV + Vancomycin IV
+
Cefotaxime or Ceftriaxone IV

36
Q

When meningitis AB do you AVOID in the Neonatal period

A

Cefotaxime or Ceftriaxone IV

37
Q

Empiric Therapy-
Healthcare-Associated Bacterial Meningitis

A

Vancomycin and Ceftazidime or
Vancomycin and Cefepime or
Vancomycin and Meropenem**

You need vanco because of all the resistance in hospitals

And a BROAD SPECTRUM one

38
Q

Aminoglycosides are

  • usually prescribed for
  • However, it is also prescribed for a and b meningitis
  • why^?
A

He told us they cover gram NEG and too big to cross BBB

HOWEVER it is included in the treatment of Meningitis by

a. Group B streptococcus
b. Listeria Monocytogenes

the reason it is added to the last two is NOT because we depend on them to act. We use it for SYNERGY**

it is given WITH ampilcillin or penicillin

THE PENicilin will punch a whole, while the amino will enter and destroy the bacteria 24 hours sooner

39
Q

Adjunctive Steroids for Meningitis

A

IV Dexamethasone is recommended for meningitis caused by:

Haemophilus influenzae in infants, children & adults
- Decrease hearing loss
Streptococcus pneumoniae in adults (some experts recommend in children)
- Lower mortality and protects against severe hearing loss

Rationale: prevent neurological damage [recall the increased pressure common in bacterial meningitis] (especially to hearing) due to inflammatory and cytokine influx after antibiotics cause lysis of bacteria and release of pro-inflammatory factors into the closed brain space

40
Q

Public Health Implications of Meningitis

- There are three pathogens for which public health concerns are brought up

A
For these N. meningitidis and H. influenzae, post exposure prophylaxis is offered
Contact tracing and they are given
Prophylaxis
  - Rifampin
  - Ceftriaxone
  - Ciprofloxacin

Vaccination

For Listeria monocytogenes
Food source- find it, restrict it to protect others.

41
Q

What is the name of the tool used to identify , assess, measure and control hazards and risk of any workplace

A

HIRAC

Hazard Identification: recognizing things which may cause injury or other harm

Risk Assessment: What is the possibility of harm if exposed to a hazard

Risk Control: Measures to reduce/eliminate harm from exposure to a hazard

42
Q

What two factors determine “risk”

A

Risk means a combination of:
the LIKELYHOOD of an occurrence of a hazardous event and
the SEVERITY of injury or damage to the health of people, property, environment or any combination of these caused by the event.

E.g., A common occurrence with minimal consequences vs
A rare occurrence with disastrous consequences

43
Q

What are the MAIN

BBP: ‘Infectious microorganisms in human blood that can cause disease in humans that should be tested for?

A

Human Immunodeficiency Virus (HIV)
Hepatitis B Virus
Hepatitis C Virus

44
Q

When do needlestick injuries occur?

- what should you do?

A

When doing a procedure using a needle:

48% of needle sticks occur during use of the item
30% after use, before disposal
3% while recapping used needle

Therefore:
Have a sharps container within easy reach
DO NOT RECAP EVER

45
Q

Engineering controls

A

Primary means of eliminating or minimizing employee exposure

Include:
Use of safer medical devices
Needleless Devices
Shielded Needle devices
Plastic capillary tubes
46
Q

Administrative controls

A

Policies, procedures and patient care practices supported by adequate resources to implement controls

Best implemented at the point of first encounter with an infected source and continued until the infected source leaves the healthcare setting or is no longer infectious

E.g., Spatial separation of persons with acute febrile respiratory symptoms such as Covid

47
Q

PPE

A

Personal protective equipment (PPE) (barrier protection)

PPE are the measures of ‘last resort’ when engineering and administrative measures cannot eliminate the risk

Gloves, gowns, masks, facial protection, eye protection, face shields / masks with visor attachments, respirators

48
Q

Standard Precautions

A

WHO
Health policy: Promote a safety climate.
Hand hygiene
ASSESS THE RISK of exposure to body substances or contaminated surfaces BEFORE any health-care activity.
Select Personal Protective Equipment based on the assessment of risk
Gloves, facial protection, gown
Prevention of needle stick and injuries from other sharp instruments
Respiratory hygiene and cough etiquette
Education of health workers, patients and visitors.
Spatial separation of persons with acute febrile respiratory symptoms

49
Q

Steps after a needle stick injury

A

Wash needlesticks and cuts with soap and water

Flush splashes to the nose, mouth, or skin with water

Irrigate eyes with clean water, saline, or sterile irrigants

Report the incident to your supervisor/occupational health

Immediately seek medical treatment

50
Q

When there is a reason to believe needle stick injury is from patient how MIGHT have HIV, what is the response?

A

When there is reason to believe the patient might have HIV, the Health Care Worker should receive Post Exposure Prophylaxis (PEP)

51
Q

PEP for HIV

A

28-day course of 3 or more Antiretrovirals (ARVs)
Start ideally within 2 hours but within up to 72 hours.
Reevaluate the exposed individual within 72 hrs. focusing on new information about the source and exposure.
PEP can reduce the risk of HIV infection by over 80%.
Adherence to a full 28-day course of ARVs is critical
Recent evidence shows PEP uptake has been insufficient:
only 57% of the people who started PEP completed the full course
Rates were even lower at 40% for victims of sexual assault.

52
Q

Hep B

  • risk from needle stick injury
  • risk if victimn is vaccinated
A

Risk from needlestick is 6-30% in non immune

If the Healthcare Worker has been fully immunized with tests confirming immunity, there is no risk of contracting Hepatitis B (lifelong protection)

Otherwise:
Depending on risk, the worker may need to receive Hepatitis B immune Globulin and/or Hepatitis B immunization.

Workers who did not respond to Hepatitis B immunization need to receive immune globulin twice.

53
Q

Hep C

  • risk of transmission after needlestick
  • response if exposed
A

Hepatitis C

Risk of transmission after percutaneous exposure is 1 in 56 (1.8%)
CDC estimates 2% to 4% of annual new Hep C infections have been health care workers exposed to blood in the workplace.

No post exposure prophylaxis exists

Exposed person needs follow up tests for HCV

Protocols vary somewhat

54
Q

Why are safety enigneered needle sticks NOT used?

A
  • the benefit is not high enough to justify the costs
  • There is BARELY a reduction in transmission

while PEP was going to reduce infection
Prevents 80% HIV
Prevents 85% Hep B

55
Q

Risks for Workers who work around water?

A

Hazards include;
Escherichia coli, Salmonella, Shigella, Campylobacter, Cryptosporidium, Giardia, Norwalk virus, and enteroviruses
May be risk for Hepatitis A depending on where the sewage comes from (e.g., waste from ships)

56
Q

What should pregnant works be concerned about contracting??

A

Parvovirus B19
Highest risk of hydrops fetalis at 11-23 wks’ gestation
Positive IgG Ab in the mother indicates immunity

Chickenpox (Varicella-zoster virus)
Can lead to a severe maternal disease/death

Rubella
Congenital rubella infection during the first 16 wks of pregnancy is associated with multiple effects (congenital rubella syndrome)

Measles
Prematurity/small birth weight infant, spontaneous abortion, fetal/maternal death

57
Q

What is the epidemiologic triad

A

Host
Infectious Agent
Environment

vs
Portal of entry
Portal of exit
Reservoir

58
Q

Examples of breaking the triad?

A

Host = Susceptible Human
Immunization

Infectious Agent
Antiseptics (kill on biologic surfaces)
Handwashing
Disinfectants: kill in environment

Environment= Favourable conditions outside the host
Physical: single patient or negative pressure rooms
Dedicated material
Mosquito nets
Containment, isolation, administrative controls, protocols, etc.
Eliminate the reservoir (e.g., air conditioners and legionnaires)

59
Q

Which are the high prevalence ifnectious diseases among immigrants?

A
Tuberculosis
Viral Hepatitis (hepatitis B and C)
HIV
Vaccine Preventable Diseases including varicella
Parasitic infections (strongyloides)
60
Q

Which infectious disease is HIGHEST in immigrants?

A

Tuberculosis (TB)

followed by hep B then hep C

61
Q

What is a big bareer in quebec to providing care for immigrants?

A

accessing INTERPRETERS**

62
Q

What is the treatment for latent TB in immigrants?

A

Short Course well tolerated Rifampin LTBI Rx

Rifampin regimens are preferable

Equal efficacy

Lower hepatoxicity
RMP vs INH
RR 0.15 (0.07-0.4)

Better completion rates (82% vs 69%)

63
Q

Chronic Hep B vs C

  • which one is more transmissible
  • which one is more severe
  • which one can you cure
  • which one can you vaccinate
A
  • which one is more transmissible: HBV
  • which one is more severe: HCV
  • which one can you cure: HCV [RNA virus]
  • which one can you vaccinate: HBV [ effective vaccine, suppressive therapy, DNA virus]

Increased death from HCC and viral hepatitis 2-4 fold
Refugee 2-fold greater risk of death
Increased hospitalizations for HBV
Those with HCV increased risk to die in hospital from HCC
HBV effective vaccine, suppressive therapy
HCV curative therapy >95%
Cost-effective to screen/treat for HBV and HCV

64
Q

Screening for HBV vs HCV

A

HBV more complex:
HBsAg, anti-HBc, anti-HBs
* DNA, lifelong. can be prevented with vaccine

HCV just one:
anti-HCV
* RNA, can be cured

65
Q

What should we be mindful of considering post arrival acquisition of HIV among immigrants, especially MSM

A

HIV occurred in 2209 migrants within 5 years of arrival in Europe
>50% of HIV cases acquired POST ARRIVAL due to risk behaviors

66
Q

Burden of Varicella in immigrants

  • who is most at risk
  • who is most at risk of hospitalization
  • when is the risk greatest?
A

***Increased susceptibility and burden of varicella in immigrants

Temperate countries [like canada] >95% immune by age 20 vs tropical ~70%

Outbreaks of varicella in immigrant esp crowded settings
Adults ↑ risk of hospitalization, death
Pregnant women higher risk and congenital and neonatal varicella

Varicella risk in immigrants highest in first 2 years

67
Q

What should you CONSIDER when treating IMMIGRANTS with dexamethasone or tociluzimab

A

RECALL these are immunoSUPPRESSING drugs
so it can lead to REACTIVATION of illnesses

so CONSIDER screening for
TB and
STRONGYLOIDES

68
Q

Which parasite has a high prevalence amount all immigrants?

A

High prevalence of Strongyloides among all immigrants*

Ubiquitous intestinal parasite in tropical environments
Most asymptomatic but persist for decades due to autoinfection
Can cause life threatening disseminated disease and hyperinfection in the presence of immunosuppression
Greatest risk: hematologic malignancy, steroids, HTLV I/II
Immigrants seroprevalence 12.2% vs 1.8% stool
Similar across all age groups, regions of origin

Consider empiric ivermectin in those from high risk countries, with immunosuppressive condition and being treated with Dexamethasone or Tociluzimab and Dexamethasone*

69
Q

TB infection vs disease

  • result on skin test
  • contagious
  • Symptomatic
A

Tuberculous infection is the carrier state

  • Non-infectious, tuberculin skin-test positive
  • Clinically latent (like hypertension, osteoporosis)
  • Hence, called latent TB infection (LTBI)

Tuberculosis (TB) is the diseased state

  • Contagious, culture positive
  • Symptomatic in many, asymptomatic also
70
Q

Organism behind TB

A

Mycobacterium is the genus

  • Most mycobacteria are harmless
  • These are called non-tuberculous mycobacteria (NTM)

Mycobacterium tuberculosis is the pathogen

  • Causes tuberculous infection and tuberculosis disease
  • Humans are the definitive host
71
Q

Rate of transmission for those exposed

A

90% exposed develop NO DISEASE

10% exposed develop disease

72
Q

TB and symbiont concept

A

M. tuberculosis is a pathogen BUT ALSO a symbiont. the longer the host lives, the longer TB gets to live, so it does not want to cause severe pathology. we are it’s reservoir.

M. tuberculosis is an “educated” pathogen. usually LOCALIZED, chronic pathology. host is ambulatory- allowing host to transmit and spread TB more.

the healthier the host is with the disease the more like the disease will spread and the pathogen will survive.

73
Q

What are the 3 different outcomes you can have after TB exposure?

A

no infection: up to 70% don’t test positive

TB infection: non contagious- latent TB, no disease

TB disease: -10% progress to disease. greater changes of disease within first year of infection. Contagious, may or may not be symptomatic

74
Q

Mode of transmission for TB

A

M. tuberculosis expelled by coughing +/- tidal breathing
Infectious droplet (called aerosol) travels through the air from patient with TB into the alveoli of the contact’s lungs
Consequence: M. tuberculosis in alveolar macrophages

75
Q

Pathogenesis of TB when

  1. it first enters
  2. once it is inside host
A

Options upon ENTRY:
a. Hostile: Kill bacteria at contact
No infection.
Tuberculin skin test negative

b. Welcoming: Permit bacterial infection + replication
Local infection established – called Ghon focus
More cells recruited to the site of the infection – generates an early ‘granuloma’: fibrous ring with macrophages and lymphocytes

Options AFTER it has entered:

Dendritic cells take bacteria via the lymphatics
M. tuberculosis is now in lymph nodes
M. tuberculosis antigens are presented to lymphocytes
Tuberculin skin test positive (cell-mediated immunity ~ 6 weeks)

Options:
a. Chronic localized lymphadenitis - containment
b. Further spread
Via lymphatics, within lungs (apex) or beyond (lymphatic TB)
Beyond lymphatics, via thoracic duct to blood
Hematogenous seeding (anywhere)

76
Q

What is the Chon Focus

A

Name for a PRIMARY TB lesion

77
Q

Chronic localized inflammatory lung process vs Disseminated TB

A

Chronic, localized inflammatory process in lung :
M. tuberculosis spills from cavity into the airways
- Patient is contagious (+/- sick)
Focal pathology is selective for both host and bacterium
- Delayed host mortality ~ 3 years median untreated
- Ensures bacterial survival (transmission)

Disseminated TB:
Naturally lethal to pathogen, and often to host
- TB meningitis is not transmissible
- Medically - more urgent

78
Q

Clinical Manifestations of TB
General
Organ specific
non contagious forms

A

General
Fever, sweats, weight loss, “consumption”

Organ specific
Pulmonary: cough, sputum +/- blood
Contagious TB, consumption, phthisis

Other, typically non-contagious forms:
ENT – Scrofula: swollen lymph nodes
Urology - Genitourinary = sterile pyuria
Orthopedics - Bone: back pain, ‘hump-back’ – a.k.a. Pott’s disease
Neurology - Meningitis: headache, obtundation
Non-specific - Miliary TB: no obvious site

N.B. ~30-40% people with culture-confirmed pulmonary TB are asymptomatic

79
Q

what does chest x ray tell you regarding TB

A

Chest radiograph
Not specific for TB.
But, rarely negative in active TB (immigration screening)

nothing specific but it HAS TO BE ABNORMAL if it is TB

80
Q

Usefulness of TB skin test for detecting TB disease?

A

NOT useful. can detect INFECTION but can not tell you if it is latent or active TB

microbiologic/histologic growth of TB would confirm active TB i think

81
Q

What stain is TB?

A

NEITHER gram postive or negative
you need an ACID FAST STAIN
[ Gram stain helps to distinguish bacteria with different types of cell walls whereas acid-fast stain helps to distinguish Gram-positive bacteria with waxy mycolic acids in their cell walls]

82
Q

PCR vs Culture for TB diagnosis

A

PCR is More sensitive than microscopy
however, Less sensitive than culture

so preference for CULTURE to diagnose TB

Use: 
a. Where culture is done, PCR is an ‘extra’ test
Specific use (e.g. when AFB smear is positive), e.g. Montreal 

b. Where culture is not done, PCR is better than microscopy
New standard for developing world (also used in Nunavik, Nunavut)

culture> PCR> microscope

83
Q

Treating TB

  • goal
  • what DOESN’T work, similar to _ disease
  • Treatment
A

Goal: Kill bugs dead
Immune response not considered (we treat the same in face of AIDS)

Multi-drug treatment required (like cancer)*
Resistance arises by selection of mutations
Resistant forms can spread:
Multi-drug resistant (MDR-TB) / Extensively-drug resistant (XDR-TB)
It takes weeks to get susceptibility data
So, we start with 4 drugs to be sure there are 2 active drugs
Standard: Isoniazid, Rifampin, Pyrazinamide, Ethambutol

‘Short-course’ treatment = 24 weeks

84
Q

What are the two types of testing for TB

  • causes of false positive
  • causes of false negative
A

Skin test:
Put antigens in the patient
- CANNOT distinguish infection from disease

false positive: non TB mycobacteria or BCG vaccination
false negative: AIDS, disseminated disease

Blood test (newer)
Interferon-γ release assays (IGRA)
Bring the patient’s lymphocytes to the antigens

85
Q

Purpose of quantiferon

A

this is a TB test

BCG vaccine can give false positive on skin test. Quantiferon can be used instead.