Flashcards in Module 5 Path Continued: Pneumonia Deck (45):
Staphylococci infections are gram + cocci that normally colonize in human skin; entero, exo-, exfoliative -toxins. What are the common species?
S. aureus (most infections caused by this)
Streptococci Infections are gram + cocci-diplo or strepto and produce hemolysis: classified into alpha and beta. Streptococcus pyogenes are streptococci infections, what are some feature of S. pyogenes?
Group A beta hemolytic; most important human pathogen
Direct damage: suppurative, cellulitis, abscess, pneumonia
Indirect damage by immune response
ex: Post-Strep Glomerulonephritis, Rheumatic heart disease and scarlet fever
Lobular Bronchopneumonia is caused by what bacteria?
Staph Aureus (only gram positive)
All are Aggressive
What is the pathogenesis of lobular bronchopneumonia?
URT infection ---- acute bronchitis --- spread of inflammatory exudate to adjacent alveoli ---- destruction of bronchioles and alveoli
(so starts in bronchus)
---no macrophages in bronchioles to clean up the debris so this leads to scarring
What patients normally get Bronchopneumonia?
Children, elderly, bedridden and immunocompromised
What do patients present with that have bronchopneumonia?
Fever, pleuritic chest pain worse on inspiration, dyspnea, productive cough with bloody sputum
What is the best investigation as well as the first investigation for bronchopneumonia?
Best = Sputum culture
Initial = X-ray (Shows patchy consolidation that is white on x-ray; remember that air is black on xray)
What are the complications of lobular bronchopneumonia?
2. Lung abscess (liquificant)
3. Pleural Thickening
4. Septicemia (leads to DIC)
Patient who are immunocompromised with bronchopneumonia will they go through the same 4 stages of pathogenesis and lobar pneumonia
will go through the first three stages however they will never go through the 4th stage which is resolution
Lobar pneumonia is caused by what bacteria?
Streptococcal Pneumonia (Gram +)
Lobar pneumonia is likely to present in what kind of patients?
In healthy young adults exposed to cold, strain or exhaustion
What is the pathogenesis for lobar pneumonia? each card will go through the steps
1. Acute Congestion: exudate rich in fibrin, RBC, Fibrin and a few PMNs in alveolar lumen
--spreads throughout the pores of Kohn to involve entire lobe; alveolar walls not damaged or destroyed
what is the second step in pathogenesis of lobar pneumonia?
2. Red Hepatization: exudate rich in RBCs, fibrin, and more PMNs -- controlled infection
What is the third step in pathogenesis of lobar pneumonia?
3. Grey Hepatization:Congestion and fibrin disappear, PMNs replaced by macrophages ---- macrophages clear debris few days later with help of antibiotics
What is the final step in pathogenesis of lobar pneumonia?
Complete resolution without scaring: 10-14 days
will resolve with or without abx, just takes longer without ABX
What is the best investigation and initial investigation for lobar pneumonia?
Best: Sputum Culture
Initial: X-ray ---consolidation
What are the signs and symptoms for lobar pneumonia?
Diphtheria is caused by what bacteria?
Corynebacterium Diptheria --- gram positive bacteria
What is the pathogenesis of diphtheria?
via exotoxin does ADP ribosylation of the elongation factor there inhibits protein synthesis
Clinically how does diphtheria present?
Sore throat (pharyngitis)
Bull Neck (massive cervical lymphadenopathy)
Diphtheria causes necrosis of mucosal cells of what?
oral pharyngeal cells
What is the pseudomembrane made of in diphtheria?
Fibrin, PMNs and necrotic debris
Why should the pseudomembrane in diphtheria not be scraped off?
It is actually attached to the mucus membranes and it is an exudate so it is full of neutrophils
What patients will diphtheria present in?
(DTAP is the vaccine)
What is a complication of Bull Neck in diphtheria?
Cervical lymph nodes drain the oral cavity and this can cause resp distress because it compresses on the trachea requiring a tracheotomy
What is the best investigation for diphtheria?
What are complications of diphtheria?
Acute Complication: Most common cause of death is respiratory failure due to bullneck
Late Complication: If you scrape the pseudomembrane this can get into the blood and 2-3 weeks later then you can get (indirect response which are immune mediated responses) myocarditis and cardiac arrhythmia's and heart failure as well as peripheral neuropathy (leads to paralysis)
Clostridium Difficile is a gram positive bacillus that is part of the normal flora of the colon. However, if a patient has a disease and is taking abx what can happen?
Broad spectrum abx eliminate normal flora of the gut that normally provides protection and this causes severe mucosal suppurative inflammation
E. coli is dead so now the clostridium difficile is just growing and growing and you will find pseudomembrane in colon called pseudomembranous colitis
Remember: exotoxin mediated because its gram +
What is Rheumatic fever?
Inflammatory disease that occurs following a strep pyogenes infection
What is the pathogenesis for rheumatic fever?
Initial streptococcal sore throat, skin infection
Cross reacting antibodies: antibodies generated to M protein (surface antigen) of the bacteria cross react with tissue glycoproteins in joints, heart, skin, etc ----> get deposited in tissues and elicit inflammatory reaction at site of deposition.
The lag period for rheumatic fever is 2-3 weeks after the initial infection. then what symptoms do you develop?
Fever, polyarthritis, carditis, chorea, skin nodules, erythema
Symptoms are not a result of bacteremia or direct damage by the bacteria
Type II hypersensitivity
What kind of "bodies" can develop in the heart?
Carditis- Aschoff Bodies
Rheumatic carditis can become what?
chronic --> mitral stenosis
Post-Streptococcal Glomerulonephritis = immune-complex mediated is due to what?
Initial streptococcal sore throat, skin infection
Post-Streptococcal Glomerulonephritis has a lag period with what symptoms?
Lag period = 1-4 weeks after the initial infection
Then develop acute malaise, fever, oliguria (low output of urine), hematuria (blood in urine) , azotemia (increased BUN, creatinine and decreased GFR) and HTN
What is the pathogenesis for post-streptococcal glomerulonephritis ?
Ab to strep is produced and circulates in blood
Strep Ags and Ab to it combine = form immune complexes that circulate in the blood
Immune complexes get deposited in the BM of the glomeruli
Activated complement and induce acute inflammation -- glomerulonephritis
Resolve spontaneously in most patients as the immune complexes are cleared up
What hypersensitivity reaction is post streptococcal glomerulonephritis?
What is the causative agent for Actinomycosis?
Actinomyces Israelii (commensal bacteria in normal flora of mouth, colon and vagina) --- gram +, filamentous bacteria
Can actinomycosis cause direct damage itself?
nope, patient needs some sort of pre existing damage to their bacteria like dental trauma and very common in alcoholics with dental trauma.
There are 4 types of Actinomycosis, each card will go through one. 1)
1) Cervico- facial (oral cavity)
---Through breach in oral mucosa- sinus tracts (connection between mouth and epithelial surface)
--Presents with fever, painful lumpy jaw
2nd type of Actinomycosis?
2) Thoracic: aspiration pneumonia
3rd type of Actinomycosis?
3) Abdomen: direct inoculation during surgery
4th type of Actinomycosis?
4) Pelvic: contaminated intrauterine devices and patients will get endometriosis (inflammation)
What kind of granules are present in Actinomycosis infection?
Sulfur granules they are yellow and they contain pus (neutrophils) and secrete protein that gels colonies of bacteria together