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Flashcards in Infectious Disease Deck (84)
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Name seven histological response patterns to infection.

1. Acute suppuration
2. Mononuclear inflammation
3. Granulomatous inflammation
4. Chronic inflammation and scarring
5. Cytopathic/cytoproliferative inflammation
6. Necrotizing inflammation
7. Little evidence of inflammation


Describe how the skin, respiratory tract, GI tract, and GU tract serve as normal, physiological barriers to infection. (4)

1. Skin (stratified squamous) - prevents pathogens from outside environment from penetrating the body
2. Respiratory tract (ciliated columnar) - sweeps pathogens from lower to upper respiratory tract
3. GI tract (columnar w/ mucous) - complex interaction with bowel flora; prevents at least some pathogens from binding, facilitates others
4. Genitourinary tract (squamous/columnar epithelia) - some pathogens express specific receptors for this cell type -> UTIs


Give three examples of acute suppurative infection in different organs.

Streptococcus pneumoniae pneumonia
Acute bacterial endocarditis (staph aureus)
E. coli pyelonephritis


Describe the basic features of Streptococcus pneumonia (4).
What are the basic properties of the infective agent?
What characteristics of the infective agent are important in causing disease?

1. Encapsulated Gm+ cocci
2. Polysaccharide capsule prevents phagocytosis by MO/PMNs
---Have anti-capsule vaccines, but not for all Ag types
3. IgA proteases inactivate mucosal Abs
4. Cell wall fragments are very proinflammatory
---Induce TNF, IL-1


Describe the pathological stages of Staphylococcus endocarditis. (5)

1. Damage to endothelial surface of heart valve (catheterization, IV drug use)
2. Fibrin deposited on valve surface
3. S. aureus bacteria seed/adhere onto fibrin
4. Local destruction of tissue, PMN infiltration (-> VEGETATION: bacteria, fibrin, PMNs)
5. Potential erosion into valve ring -> hemodynamic decompensation -> death


Describe the gross (4) and histological (3) changes of infections with Mycobacterium tuberculosis.

--Yellowish patches in lung in primary
--Advanced: cavitary lung disease (spreads everywhere in upper lobes, caseous necrosis -> liquefaction of parts of lung
--White, cheesy-looking huge granulomas everywhere infection spreads
--Miliary tuberculosis: white dots everywhere (all are granulomas)

--Caseation = homogenous pink stuff
----Sometimes surrounded by fibrosis


Define normal flora. What advantages do they provide?

A very complex mix of organisms that, in general, are beneficial
Many pathogens unable to get a foothold when our normal microbiome is present
Antibiotics -> dead microbiome -> susceptability to disease


Distinguish colonization vs. invasion, including the two types of invasion.

Colonization: not causing disease, but present
--Include normal flora, potential pathogens, and opportunistic pathogens

--Tissue invasion = right through epithelium
--Intracellular invasion = get inside cells and live in them
----Active: get in on their own, actively penetrate host cells (ex. Toxoplasmosa gondii)
----Endocytosis/phagocytosis: take advantage of host mechanisms (ex. Gm-s)


Distinguish potential pathogens, obligate pathogens, and opportunistic pathogens. Give an example of each.

Potential pathogens: organisms that can cause disease in normal hosts
--Some may colonize and not cause disease, but CAN cause disease without immunosuppression
--Ex. Streptococcus pneumoniae (can cause disease or colonize)

Obligate pathogens: subcategory of potential pathogens that always cause disease; not common
--Ex. Bordatella pertussis (if present, causes disease)

Opportunistic pathogens: require opportunity (i.e. immunosuppression) to cause disease
--Ex. Pneumocystitis jirovecci (widely disseminated in people, causes pneumonia only in setting of failed cell-mediated immunity)
--Ex. CMV (no disease/mild mono in most, organ damage/systemic infection in immunocompromised)


List 5 virulence determinants (toxins, capsule, adhesins, enzymes, nutritional factors) and what they do.

Aka virulence factors

1. Toxins:
--Endotoxin: LPS, a powerful immune modulator
--Exotoxins: secreted proteins that may mimic intracellular signaling molecules
2. Capsule: polysaccharide; prevents phagocytosis; poor immunogen
3. Adhesins: allow adherance to cell surfaces or ECM; important in colonization
4. Enzymes: protease, collagenases, phospholipases; disrupt cells and tissues
5. Nutritional factors: iron binding proteins, hepcidin -> control of iron, steals it from host


Acute suppurative pneumonia by S. pneumoniae:
In general, what does the infection do to tissues? List the four general stages.

Infection = tons of neutrophils! LOBAR pneumonia with CONSOLIDATED lung tissue

1. Edema
2. Acute inflammation
3. Consolidation
4. Resolution


Acute bacterial endocarditis:
What are the basic properties of the infective agent?
What characteristics of the infective agent are important in causing disease?

STAPHYLOCOCCUS AUREUS: pyogenic (pus-causing) Gm+ coccus

Has multiple virulence factors encoded by pathogenicity island
--Coordinately induced by secreted peptide -> staph in groups turn each other on


Acute suppurative inflammation: definition and examples (3)

Acute inflammation CHARACTERIZED BY PUS (neutrophils and their debris + bacteria + macrophages)

Examples: Pneumococcal pneumonia, S. aureus endocarditis, E. coli pyelonephritis


Mononuclear Inflammation: definition and example

Example: S. typhi infection

Where inflammation is marked by presence of MACROPHAGES and LYMPHOCYTES


Granulomatous Inflammation: definition and example

Form of inflammation, usually chronic, marked by formation of GRANULOMAS
--Caseation necrosis
--Tissue destruction

Example: tuberculosis


Cytopathic/Cytoproliferative Inflammation: examples (3)

Influenza A


Necrotizing Inflammation: definition and examples (2)

Inflammation with an actively necrotizing pathogen that destroys tissue

Examples: Entamoeba histolytica, pseudomembranous colitis


Chronic inflammation and scarring: examples (2)

Lung abscess and empyema from mixed bacterial infection
Schistosomiasis (with granuloma)


Typhoid fever: list the causative agent and 6 steps of pathogenesis. How long does it last? Is diarrhea involved?

Caused by S. typhi
Lasts about 1 month
Diarrhea in late infection

1. Ingestion
2. Survival in stomach
3. Invasion of small bowel through invasion of MOs in Peyer's patches
4. Spread through lymphatics
5. Bacteremia -> spreads through blood
6. Reinfects GI -> ulceration, bleeding, perforation in GI tract


Peyer’s patch/reticuloendothelial cells

Peyer's patch = specialized lymphoid site in small bowel
--Contains MOs, DCs, and lymphocytes
--Focus of intense inflammation and necrosis in S. typhi infection


Salmonella typhi:
What are the basic properties of the infective agent?
What characteristics of the infective agent are important in causing disease?

INTRACELLULAR Gm- ENTERIC bacteria with flagella and pili
Exclusive human host - transmitted by fecal contamination of water/food

Invades and survives in MOs using its T3SSs
Has endotoxin -> sepsis


Define granuloma. List its histological features. (5)

Highly organized FOCUS OF IMMUNOLOGIC CONTROL elicited by some intracellular organisms
--Multinucleated GIANT cells commonly found at center
--EPITHELIOID cells arranged near giant cells
--Rim of lymphocytes around whole thing
--Center liquifies -> caseous necrosis
MOs, lymphocytes move in/out over time -- dynamic


Mycobacterium tuberculosis/tuberculosis:
What are the basic properties of the infective agent?
What characteristics of the infective agent are important in causing disease?

Acid fast intracellular mycobacteria (waxy cell wall makes it hang onto dye even when strongly decolorized)

-Prevents acidification of phagosomes so it can multiply in them
-Induces granulomas via the glycolipid Lipoarabinomanan -> inhibits MO activation


What is an epithelioid cell?

Large pink macrophage with increased amount of cytoplasm
Induced by cytokines
Look "epithelioid" because of all the pink cytoplasm


Caseation (Caseous necrosis): what is it? What does it look like on a gross and histologic level?

Generally, the gross appearance of a granuloma that has been drive past the stable stage

Gross: looks like white cheese, often with liquid cavity in center

Histologic: homogenous pink stuff


What is meant by "consolidation"? What distinguishes red and gray hepatization?

Generally refers to process in lobar pneumonia associated with S. pneumoniae
Lobe of lung completely solidified - no sponginess, everything filled with pus and fibrin

Red hepatization = RBCs in infiltrate
Gray hepatization = no RBCs in infiltrate


Pneumonia from S. pneumoniae:
Describe the edema stage. (4 features)

Serous exudate: FIBRINOGEN-containing fluid leaks from vessels
Thickened alveolar walls
Congested vessels
Damage to endothelial cells starts


Pneumonia from S. pneumoniae:
Describe the acute inflammation stage. (5 features)

Recruitment of LOTS OF PMNs and platelets, some MOs
Leak of RBCs possible
Activation of complement and coagulation cascades
Polymerization of FIBRIN
Vessels still congested


Pneumonia from S. pneumoniae:
Describe the consolidation stage. (1 feature)

Lung tissue becomes firm and red or gray (=yellow) in color


Pneumonia from S. pneumoniae:
Describe the resolution stage. (2 features)

Restoration of architecture by MACROPHAGE cleanup of inflammatory infiltrates
Vessels still congested