Respiratory Tract Infections

Front 1

How is Group A Streptococci spread?

Back 1

-droplets
-affects young children (1-15)
-usually occurs winter thru spring (school outbreaks possible)

Front 2

What are Group A Streptococci virulence factors?

Back 2

>M-protein- antiphagocytic; anit M protein antibodies play role in rhematic fever
>hyaluronic acid CAPSULE
>Pyrogenic exotoxin-acts as SUPERANTIGEN
>Degradative enzymes- hemolysins, proteases, hyaluronidase, adn DNAse

Front 3

Group A Streptococci symptoms

Back 3

pharyngitis
shotty lympadenopathy
fever
>scarlet fever is often seen in patients with GAS pharyngitis; organism produces a streptococcal pyrogenic toxin

Front 4

Group A Streptococci prevention

Back 4

>treated with penecilin G to prevent Rheumatic fever
> macrolides given to people allergic to penicillin G
> no vaccines available

Front 5

Group A Streptococci invasive disease

[necrotizing fasciitis]

Back 5

> seen as a complication to chicken pox
> virulence factors allow the organism to spread throughout the tissue
> may cause toxic shock if the organism turns into a superantigen
> HIGH MORTALITY- needs surgical debridgement

Front 6

Rheumatic fever

Back 6

> occurs avter GAS pharyngitis
> antibodies against M protein cross reacting with antigens in the heat valves or muscle causes tissue damage
>diagnosis--> Jones Criteria (nno)
>,can be prevented if we treat GAS pharyngitis

Front 7

How is Streptoccous pneumoniae spread?

Back 7

droplets
> it can colonize upper respiratory tract
>common in winter months
> problematic in very young and very old basically those who are immunodeficient (asplenic individuals and sickle cell patients)
-causes Pneumococcal pneumonia

Front 8

Streptoccous pneumoniae virulence factors

Back 8

capsule-prevents phagocytosis
pneumolysis-cytolysin that acts on alveolar epithelial cells and pulmonary endothelial cell; induces inflammation

Front 9

Streptoccous pneumoniae treatment

Back 9

> PENICILLIN
>Vaccines: 13 valent conjugated polysaccharide vaccine used in children for prevention

Front 10

influenza A infection with 2009 H1N1 virus facts

Back 10

•an acute illness with aching muscles, a characteristic dry hacking cough, and headache; caused by a virus which infects the cells lining the air passages
•spreads rapidly from person to person by inhalation of tiny droplets from the exhalations of infected people
•three types; types A and B are important in human health, especially A
•ranks among the greatest of the unconquered epidemic diseases that affect humans

Front 11

Tuberculosis (Mycobacterium tuberculosis) symptoms

Back 11

fevers, night sweats, increased cough, hemopytsis, weight loss, disseminate to other organs

Front 12

Tuberculosis (Mycobacterium tuberculosis) epidemiology

Back 12

> chronic, CA pneumonia
> spread by aerosol
> 90% asymptomatic
> immigrants, urban poor, homeless, alcoholics, and prison inmates at risk

Front 13

Tuberculosis (Mycobacterium tuberculosis) pathology

Back 13

Initial infection- organism inhaled in small droplet
Tubercle bacilli taken up by macrophage; survives and slowly multiples (generation time 24 hours)
After three weeks, cell mediated immunity emerges
CD4 cells activate macrophages to kill tubercle bacilli and cause granulomatous inflammation
Lesion known as Ghon complex is formed
Center of lesion has caseous (cell death) inflammation
Free bacilli or organism in macrophages may drain to regional lymph nodes causing necrosis there as well
Organism may remain viable in these lesions
This is the latent stage of the infection
Reactivation may occur in immunocompromised patients
Reactivation occurs in patients with waning immunity
Pathology usually seen is an expansion of the area of necrosis
Erosion of lesion into bronchi may result in cavity formation
Erosion into blood vessels may result in hemoptysis

---reactive

Front 14

Tuberculosis (Mycobacterium tuberculosis) virulence

Back 14

-inhibition of phagosome-lysosome fusion
-inhibition of phagosome acidification
-resistance to reactive oxygen intermediates
-reactive nitrogen intermediates
-inhibition of antigen presentation

Front 15

MDR-TB

Back 15

typically resistant BOTH isoniazid (INH) and rifampin as well as other first line drugs

Front 16

Pre-XDR

Back 16

MDR and resistant to one or more 2nd line injectable agents or a fluoroquinolone- we recently saw a patient with pre-XDR-TB-a 28 yo old Filipino immigrant who died of miliary TB-underlying disease-Lupus

Front 17

XDR-TB

Back 17

MDR-TB that is also resistant to any fluoroquinolone and one injectable 2nd line drug (capreomycin, kanamycin, amikacin)