Microbiology Of URI's Flashcards

1
Q

Normal protective body mechanisms against URI/LRIs

A

Mucocillary apparatus

Dendritic cells (DCs)

Alveolar macrophages

IgG

Compliment

Surfactant

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2
Q

Mucocillary apperatus specifics

A

Mucus traps pathogens in the respiratory system and either brings it down to the stomach or cough it out via the cough reflex

Mucus also contains enzymes and IgA which degrade bacteria an provide a bacteriostatic environment to most pathogens

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3
Q

Dendritic cell specifics

A

Sense and catch pathogens and bring them to draining lymph nodes to activate adaptive immune responses

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4
Q

Alveolar macrophage specifics

A

Catch particles in the lower respiratory tract that managed to avoid all other defenses

  • phagocytize them
  • also secrete ROS and bacteriocidal enzymes
  • synthesis cytokines

Are primary phagocytes of the innate immune system

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5
Q

Common virus agents in the upper respiratory tract infections

A

Adenovirus

Rhinovirus

Parainfluenza virus

RS virus

Coxsakie virus

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6
Q

Common Bacterial pathogens that infect them upper respiratory tract

A

GAS

GCS

Gonorrhea

Diphtheria

Chlamydia

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7
Q

Rhinitis

A

Infection of the nasal cavity
- produces variable cold like symptoms

Most common symptoms are:

  • nasal stuffiness
  • sneezing
  • runny nose
  • sore throat

Pathogenesis

1) Virus attachment initiates viral replication
2) Lysis cells once replication is complete
3) lysis of cells spreads to other respiratory cells causing destruction and further infection

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8
Q

What are the most common infections of the nasopharynx?

A

Virus pathogens
- rhinoviruses and coronavirsues make up 50%

Very rare for bacterial but still possible

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9
Q

Rhinoviruses

A

MOST COMMON CAUSE OF COLDS

Are small, un-enveloped viral particles
- single-stranded (+)-sense RNA
- optimal temp = 33C
Replicates and spreads locally as well as is shedded in nasal secretions

Secretory IgA is the prime mover in destroying the virus
- also develops the symptoms

Location of rhinovirus in people who are infected

1) hands (why washing hands is sooo important)
2) nose
3) saliva

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10
Q

Bacterial pharyngitis vs viral pharyngitis

A

Bacterial:

  • medical intervention needed
  • swollen uvula
  • swollen lymph nodes w/ white spots
  • gray furry tongue apperance
  • throat redness
  • this is usually strep throat
  • GAS or GCS are causative agents

Viral:

  • self-limiting and home care only
  • swollen tonsils w/out white spots
  • throat redness
  • almost always shows w/ additional nasal issues
  • most commonly a rhinovirus
  • can also be coxsackie, EBV or RS viruses
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11
Q

Herpangina vs hand/foot/mouth disease

A

Both are caused by coxsackie viruses

Herpangina:

  • Group A coxsackie virus
  • abrupt onset of fever
  • sore throat w/ cold sore looking lesions on soft palate
  • dysphagia and malaise
  • may show vomiting also
  • most common in children between 1-7 yrs

Hand/foot/mouth

  • generalized coxsackie virus
  • almost exactly like herpangina except also produces the following
  • skin rashes
  • blisters on hand and feet
  • also usually affects children 1-7
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12
Q

Epstein Barr virus

A

Member of herpes

  • replicates in oropharyngeal epithelial cells
  • transmits via saliva and local infection in the mouth/pharynx and larynx
  • disseminates through the body via the reticuloendothelial system and often infects B-cells

Almost always is asymptomatic in innate/latent phase

Reactivating phase produces most of the symptoms of mono

  • fever
  • lymphadenopathy primarily posterior regions
  • severe malaise
  • sore throat
  • only differ enforcement between this and mono symptom wise is the lymphadenopathy is anterior and splenomegaly is often reported*

Most common in the following 2 age groups

1) children between 1-6
2) young adults between 14-20

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13
Q

Primary EBV infections pathogenesis

A

Infects B-cells eventually and triggers abnormal replication

  • produces heterophile antibodies (non-specific IgM antibodies) which go on to destroy and target RBCs and other tissues
  • heterophile antibodies are tested via direct agglutination of multiple blood samples (will bind to all)

Clinical symptoms arise based on T-cells activating in response to the abnormal B-cells

After “curing” EBV established a latent infection in memory B-cells and their future generations
- this allows virus to become reactivated in the future if it is triggered properly

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14
Q

Types of antibodies specific to EBV and the stage at which they are the most prevalent

A

Anti-EBV IgM
- most prevalent in incubate/acute phases

Viral capsid antigen IgG
- most prevalent in acute and convalescence stages

Anti-EBV IgG (EA-D IgG)
- most prevalent in acute phase

Anti-EBV IgG (EBNA-1 IgG)
- most prevent in the convalescence stage

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15
Q

How to diagnose EBV from testing

A

obviously clinical presentation must match first

Lab results

  • atypical lymphocytes (abnormal appearance with bleeding of the cell membrane)
  • presence of heterophile antibodies
  • presence of specific EBV antibodies
  • liver function tests show high liver enzymes

note if > or = 10% atypical lymphocytes are present in blood smears, it is diagnostic of mono

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16
Q

What are the two types of cancers associated with EBV infections

A

Burkitt’s lymphoma and nasopharyngeal carcinomas

17
Q

Layngotracheitis

A

Infections of the layrnx and are trachea
- most common are parainfluenza and RSV viruses

Leads to croup most commonly

18
Q

Parainfluenza subtypes and what they cause

A

note for all of these the incubation period is 2-7 days

HPIV-1/2 = croup

HPIV-3 = bronchiolitis, bronchitis and pneumonia

HPIV-4 = severe respiratory tract illness

  • infections are ALWAYS more severe in elderly and immunocompromised. Also you can be infected more than once a lifetime by each subtype (dont gain immunity) *
19
Q

Mumps

A

Symptoms

  • parotitis (swollen parotid glands)
  • fever and headaches
  • malaise
  • dysphagia and loss-o-appetite
  • pain with deglutition
  • possible CNS involvement
  • orchid is may be present in 1/3 of patients (testie inflammation)

Adults are most seriously affected

Incubation period is 16-18 days with symptoms showing 3-5 days after