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Pathology - Quiz 2 > Infectious Disease > Flashcards

Infectious Disease Flashcards

These lectures cover a selection of infections that present examples of various types of responses in tissues and organs. They are practical illustrations of mechanisms of inflammation. Use these examples to understand how infective agents in the lecture and reading cause disease, and how the disease manifests in tissues. Specifically: What are the basic properties of the infective agent? What characteristics of the infective agent are important in causing disease? What does the infection

1
Q

Name seven histological response patterns to infection.

A
  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
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2
Q

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

A
  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
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3
Q

Give three examples of acute suppurative infection in different organs.

A

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

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4
Q

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?

A
  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
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5
Q

Describe the pathological stages of Staphylococcus endocarditis. (5)

A
  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
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6
Q

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

A

Gross:

  • -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)

Histological:

  • -Granulomas!
  • -Caseation = homogenous pink stuff
  • —Sometimes surrounded by fibrosis
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7
Q

Define normal flora. What advantages do they provide?

A

Microbiome
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

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8
Q

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

A

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

Invasion:

  • -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)
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9
Q

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

A

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)
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10
Q

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

A

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
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11
Q

Acute suppurative pneumonia by S. pneumoniae:

In general, what does the infection do to tissues? List the four general stages.

A

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

  1. Edema
  2. Acute inflammation
  3. Consolidation
  4. Resolution
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12
Q

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

A

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

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13
Q

Acute suppurative inflammation: definition and examples (3)

A

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

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

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14
Q

Mononuclear Inflammation: definition and example

A

Example: S. typhi infection

Where inflammation is marked by presence of MACROPHAGES and LYMPHOCYTES

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15
Q

Granulomatous Inflammation: definition and example

A

Form of inflammation, usually chronic, marked by formation of GRANULOMAS

  • -Caseation necrosis
  • -Liquefaction
  • -Tissue destruction
  • -Hemorrhage

Example: tuberculosis

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16
Q

Cytopathic/Cytoproliferative Inflammation: examples (3)

A

Influenza A
Measles
Cytomegalovirus

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17
Q

Necrotizing Inflammation: definition and examples (2)

A

Inflammation with an actively necrotizing pathogen that destroys tissue

Examples: Entamoeba histolytica, pseudomembranous colitis

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18
Q

Chronic inflammation and scarring: examples (2)

A

Lung abscess and empyema from mixed bacterial infection

Schistosomiasis (with granuloma)

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19
Q

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

A

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
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20
Q

Peyer’s patch/reticuloendothelial cells

A

Peyer’s patch = specialized lymphoid site in small bowel

  • -Contains MOs, DCs, and lymphocytes
  • -Focus of intense inflammation and necrosis in S. typhi infection
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21
Q

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

A

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

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22
Q

Define granuloma. List its histological features. (5)

A

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

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23
Q

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

A

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
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24
Q

What is an epithelioid cell?

A

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

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25
Q

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

A

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

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26
Q

What is meant by “consolidation”? What distinguishes red and gray hepatization?

A

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

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27
Q

Pneumonia from S. pneumoniae:

Describe the edema stage. (4 features)

A

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

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28
Q

Pneumonia from S. pneumoniae:

Describe the acute inflammation stage. (5 features)

A

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

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29
Q

Pneumonia from S. pneumoniae:

Describe the consolidation stage. (1 feature)

A

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

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30
Q

Pneumonia from S. pneumoniae:

Describe the resolution stage. (2 features)

A

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

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31
Q

Pneumonia from S. pneumoniae:

What is the end result for the lung?

A

No damage to alveolar walls!

Lung CAN fully recover once junk is cleaned up

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32
Q

Briefly describe endocarditis. What causes the subactute form? Acute form?

A

Endocarditis: infection of heart valve
–Caused by lots of different bacteria

Subacute (indolent, slow) due to oral streptococci
Acute due to Staph aureus

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33
Q

Acute bacterial endocarditis from S. aureus:
What does the infection do to tissues?
What is the characteristic pattern of cellular response to the infection?

A

Results in vegetation of fibrin, PMNs, and bacteria that damage tissue

Cells = NEUTROPHILS

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34
Q

Briefly describe complications of acute bacterial endocarditis from S. aureus.

A

Vegetation may break off pieces -> travel through bloodstream -> lodge in organs throughout body (lung, kidney, peripheral vessels, skin)

Leads to infarction and inflammation wherever it lodges

35
Q

What is pyelonephritis? What most commonly causes it?

A

Bacterial infection of the kidney
Typically caused by ascending infection from bladder (lower UTI -> kidney)
May become chronic -> renal failure

Caused by Gm- ENTERIC RODS (most common = E. coli)

36
Q

Pyelonephritis:
What are the basic properties of the infective agent?
What characteristics of the infective agent are important in causing disease? (3)

A

E. coli: Gm- enteric rod

  • Facultative (anaerobic/aerobic)
  • Some strains can adhere to urinary epithelium, colonize urethra -> increased risk of UTI -> ascend UT -> infection in interstitium and renal tubules
37
Q

Pyelonephritis by E. coli:
What does the infection do to tissues?
What is the characteristic pattern of cellular response to the infection?

A

Gross appearance: white patches = areas of acute inflammation
Causes infection in interstitium and renal tubules (glomeruli spared)
—See TONS of PMNs and bacteria

38
Q

List three complications of E. coli pyelonephritis.

A

Papillary necrosis
Pyonephrosis (pus in renal pelvis)
Perinephric abscess

39
Q

Typhoid fever from S. typhi:

What does the infection do to tissues?

A

General = MONONUCLEAR INFLAMMATION

  • Rose spots on abdomen: lesions of mononuclear inflammation
  • Small bowel lesions: infects Peyer’s patches, then ulcerate through
  • –Can lead to hemorrhage or leaked bowel contents -> peritonitis
  • –Serosa greatly thickened, edematous
  • –Epithelium harmed via necrosis
40
Q

Typhoid fever from S. typhi:

What is the characteristic pattern of cellular response to the infection?

A

Mostly MACROPHAGES responding, some lymphocytes
–NO neutrophils
Macrophages induced to phagocytose S. typhi

See necrosis and inflammation

41
Q

What is meant by “acid fast”?

A

Acid fast test = Gm stain using an acid-alcohol decolorizer

—Decolorizes even Gm+ organisms, but not M. tuberculosis

42
Q

Tuberculosis:

What is the characteristic pattern of cellular response to the infection?

A

DTH: CD4 cells -> TNFa and IFNy secretion -> MO activation -> granuloma formation
–CD8 cells can lyse infected macrophages

43
Q

Describe what is meant by saying, “The balance of cytokines is key in granulomatous inflammation.”

A

Alleles of leukotriene hydrolase control balance of TNF

  • –Too little TNF: uncontrolled growth of TB, disseminated infection, death
  • –Too much TNF: overgrowth of granulomas, tissue destruction
  • –Just right TNF: stable granuloma
44
Q

Tuberculosis:

Distinguish between primary and secondary infection.

A

PRIMARY: get granuloma near bronchus and granuloma on periphery
—Stay dormant or calcify unless cell-mediated immunity fails (-> secondary)

SECONDARY: MILIARY tuberculosis
—Infection diffuses via bloodstream to lung, liver, spleen, adrenals, bone, meninges, lymph nodes

45
Q

Diagram what an “empyema” is anatomically and state the most frequent cause of such infection.

A

Cause: mixed aerobic and anaerobic bacteria (from aspirated upper respiratory flora)

Bacterial infection of lung -> acute suppurative inflammation -> tissue destruction -> ABSCESS
–Spreads to pleura -> EMPYEMA

46
Q

Define empyema.

A

A collection of pus in the space between the lung and the inner surface of the chest wall (pleural space)
Composed of pus, fibrin, inflammatory cells

47
Q

Define lung abscess

A

Walled off fibrous cavity with liquefied central cavity

48
Q

How does an empyema resolve? What is the result?

A

Resolves by draining through bronchus or chest wall

Result: FIBROSIS; lung tissue never returns to normal

49
Q

Lung abscess and empyema:

What is the characteristic pattern of cellular response to the infection?

A

Aerobic/anaerobic bacteria -> recruitment of MOs, lymphocytes, and plasma cells, which surround the areas of bacterial growth

50
Q

Lung abscess and empyema:

What are the gross (1) and histological changes associated (3)?

A

Gross:
–Rather than gray pleura, see gross shaggy yellow-pink empyema (pus, fibrin, inflammatory cells)

Histologic:

  • -(see layers:) Normal lung tissue – Granulation tissue – Abscess (purple stuff/cavity) – Empyema
  • -Granulation tissue: new vessels, young fibroblasts
  • -ABCESS: see giant purple areas of chronic inflammatory cells breaking stuff down and forming a cavity
  • -Empyema: fibrin, bacteria, inflammatory cells off to the edge of the purple areas
51
Q

Entamoeba histolytica:
What are the basic properties of the infective agent, including its life cycle (4 steps)?
What characteristics of the infective agent are important in causing disease?

A

Protozoan with infectious cyst, invasive trophozoite
–Amoeba is motile! Can help distinguish it from other amoebas

Life cycle:

  1. Cyst lingers in water, gets ingested
  2. Cyst breaks out in intestine, -> feeding stage (trophozoite)
  3. Trophozoite eats the colon, can also infect liver, lung, and brain
  4. Poop out cysts

Amebic surface lectin allows trophozoite adherence to colonic epithelium, invasion, complement resistance

52
Q

Contrast the granulomas caused by shistosome infection with those caused by mycobacterium tuberculosis. (3)

A

Shistosome differences from tuberculosis:

  • -MAJOR cell in early response AND in granuloma is EOSINOPHIL (rather than neutrophil)
  • -Often see schistosome egg with dots in it (larva) in the middle of granuloma
  • -Get enormous amounts of scar formation -> chronic disease
53
Q

Pseudomembranous colitis:

What are the basic properties of the infective agent?

A

Caused by C. difficile: toxin producing, Gm+, spore-forming anaerobic baccilus

Widespread in nature, spores stable in environment
–Colonization of large bowel/growth after disturbance of normal microbiome

54
Q

Schistosoma/Schistosomiasis:
What are the basic properties of the infective agent? Very briefly discuss the infectivity of its life stages.
What characteristics of the infective agent are important in causing disease?

A

A species of tropical freshwater bloodfluke (worm) - get it by wading in freshwater

  • -Invasive larva penetrates skin
  • -Adults live in bloodstream in mesenteric veins: elicit no inflammatory reaction, but produce EGGS
  • -EGGS: -> eosinophilic infiltrate, granulomas, and dense fibrosis
55
Q

Influenza A:

What are the basic properties of the infective agent? What do hemagglutinin and neuraminidase do?

A

RNA virus; can infect both animals and humans
Segmented genome -> antigenic variation -> epidemics

Hemagglutinin -> fusion with host cell
Neuraminidase -> allows virus to uncoat

56
Q

Hyaline membrane: what is it and when is it seen?

A

Hyaline = something that is clear, glassy, eosinophilic

Seen in viral pneumonia: proteinaceous fluid exuded into interstitium of lung coagulates, forms pink glassy-like substance

57
Q

Cytokine dysregulation: what is it and when is it seen?

A

High cytokine levels and disregulation of cytokine balance -> lack of control of virus replication -> massive damage in lung -> systemic damage
–Looks a lot like acute bacterial pneumonia: lesions involve large amounts of lung and fill alveoli; TNF produced in very large amounts

Seen in avian influenza, a severe form that moves very rapidly (can kill within hours to days)

58
Q

Measles/Rubeola:
What are the basic properties of the infective agent?
What characteristics of the infective agent are important in causing disease? (symptoms)

A

RNA virus; one strain without antigenic variation
Hemagglutinin binds to many cell types by a complement regulatory protein (don’t need to know name)

Symptoms: rash, especially around mouth and eyes; diagnostic mucosal Koplik spots

59
Q

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

A

DNA herpesvirus
Opportunistic disease: seen in immunosuppressed, AIDS, congenital infections

Infection of epithelial and endothelial cells

  • -Organs most involved are lungs, liver, kidney, GI tract, CNS, retina
  • -Can cause pneumonia, focal necrosis in many organs, ulceration of intestine
60
Q

Know the non-bacterial agents that can induce giant cells (some viruses, yeast/fungi, parasites and their eggs).

A 
Cytomegalovirus
TB (bacteria)
Schistosoma
Cryptococcal meningitis
Measles
61
Q

What cytokines are relevant to schistosomiasis? How do these contribute to fibrosis?

A

IL-4, IL-5, IL-13

IL-4, IL-13 act on macrophages, push alternative pathway -> macrophages led to produce lots of collagen!

62
Q

Cryptococcal meningitis:

What are the basic properties of the infective agent?

A

Example of an infectious agent with LITTLE INFLAMMATION

Caused by Cryptococcus neoformans: encapsulated yeast

  • -Found worldwide in high N soils (lots of bird droppings)
  • -Aerosol spread
  • -Polysaccharide capsule = virulence factor, also useful for diagnosis
  • -NO toxins
63
Q

Are yeasts Gram + or -?

A

All yeasts are Gm+

64
Q

Malaria:

What are the basic properties of the infective agent? Briefly explain its life cycle.

A

See LITTLE INFLAMMATION

Caused by a number of organisms in Plasmodium genus
Most virulent = Plasmodium falciparum

Life cycle:

  • -Infectious form in mosquito is injected into blood by bite, infects hepatocytes
  • -Parasite form matures in liver, breaks out and infects RBCs
  • -Infected RBCs lyse, release new infectious forms, which attach to and invade RBCs
  • -Some gametocytes eventually form, get transferred to mosquito
65
Q

Malaria:

What characteristics of the infective agent are important in causing disease? List some characteristics of the disease.

A

Binds RBC to endothelium via integrin and thrombospondin receptors -> local clogging of small vessels, release of high levels of cytokines -> breakdown of vessels and acute organ dysfunction

Disease: periodic fevers coordinated with RBC lysis

  • -Fever
  • -High parasitemia -> “ring forms” of condensed chromatin and blue cytoplasm in RBCs
  • -Severe anemia
  • -Renal failure
  • -Cerebral dysfunction (may evolve very rapidly)
  • -Pulmonary edema
  • -Death
  • -Immunity doesn’t persist long, reinfections are common
66
Q

Malaria:
What does the infection do to tissues? (gross and histological changes)
What is the characteristic pattern of cellular response to the infection?

A

Gross:

  • -Congestion/enlargement of spleen and liver
  • -Cerebral edema

Histological:

  • -Cerebral malaria: small vessels filled with parasitized RBCs with ring hemorrhages, look like brownish sludge
  • -High parasitemia -> “ring forms” of condensed chromatin and blue cytoplasm in RBCs
  • -Little inflammatory infiltrate
  • -Chronic malaria: deposition of malaria pigment from hemoglobin digestion (lots of brown stuff) gets entrapped in MOs
67
Q

How is malaria diagnosed?

A
  • -Examination of blood films
  • —Thick smear: smear lots of RBCs, lyse them, look for parasites

(DO NOT learn all blood forms)

68
Q

Cryptococcal meningitis:

What characteristics of the infective agent are important in causing disease? Briefly describe the disease.

A

Disease:

  • -Causes a fairly common respiratory infection in most
  • -Immunosuppression -> dissemination to meninges, bone, skin
  • —Insidious onset (weeks to months) of chronic meningitis, hydrocephalus
69
Q

Cryptococcal meningitis:

What does the infection do to tissues? (gross and histological changes)

A

Gross:

  • -Infection of meninges can look like a jelly-like substance
  • -Can disseminate to skin -> raised, umbilicated lesions

Histological:

  • -If capsule or melanin (which these yeast produce) is stained, see lots of yeast in infected tissue with very little acute inflammation
  • -Skin: produces clear spaces in the dermis in H&E staining
70
Q

Cryptococcal meningitis:

What is the characteristic pattern of cellular response to the infection?

A

Cell response:

  • -Little acute inflammatory response
  • -Macrophages phagocytose the yeast (can see as clear blebs in MOs)
  • -Requires cell-mediated immunity to contain it
  • -Loose granulomas after a long time (not pretty, tough to spot)
71
Q

How is cryptococcal meningitis diagnosed?

A

Diagnosis:

  • -Grow yeast in culture: will look brown if grown with enough tryptophan
  • -Stain and India ink preparation (yeast capsule keeps dark ink away)
  • -Ag detection of secreted polysaccharide in CSF or serum - few cross reactions, fastest and easiest way to make diagnosis
72
Q

Cytomegalovirus:
What does the infection do to tissues? (histological changes) What is the characteristic pattern of cellular response to the infection?

A

Histological: Cytopathic/cytoproliferative effect: large intranuclear inclusion within enlarged cells

  • -Infected cell grows -> huge inclusion of viral DNA within nucleus
  • -Look like large cells with very dark nuclei and slight clearing around nucleus (owl’s eye cells)
  • -These cells eventually die -> necrosis
73
Q

How is cytomegalovirus diagnosed?

A

Diagnosis of latent infection vs disease: measure viral load by antigen or molecular detection (qPCR)

  • -Disease = higher levels than latent infection
  • -Most people are latently infected and will have small amounts of virus
74
Q

Measles/Rubeola

What does the infection do to tissues? (histological changes)

A

Pneumonia:

  • -Peribronchiolar and interstitial lymphocytic and mononuclear infiltrate
  • -Lymphoid hyperplasia
  • -Multinucleate syncytial cells in lung, lymph nodes
  • —Created by multiple-cell fusions of MO lineage (vs TB: formed by single MO that enlarges and replicates its nucleus)
  • -Alveoli pretty much clear
75
Q

Measles/Rubeola:

What is the characteristic pattern of cellular response to the infection?

A

Multiplies within epithelial and mononuclear cells
–Growth controlled by T cell response
–Antibody protects against infection (not disease)
Suppression of cell-mediated immunity (including by malnutrition) increases severity of disease
–Rash requires cell-mediated immune response

76
Q

Influenza A:

What characteristics of the infective agent are important in causing disease? What is secondary pneumonia?

A

Primary viral pneumonia:

  • -Edema
  • -Major systemic symptoms
  • -Necrosis of ciliated respiratory epithelium
  • -Lymphocytic infiltrates in the submucosa
  • -SETUP for secondary pneumonia
  • -Virus attaches to cilia of respiratory cells

Secondary bacterial pneumonia: frequently with bacteria that don’t normally cause pneumonia without influenza A

  • -Pathology: acute supperative inflammation that fills up alveoli
  • -Commonly caused by S. aureus
77
Q

Influenza A:
What does the infection do to tissues? (gross and histological changes)
What is the characteristic pattern of cellular response to the infection?

A

Gross:
–Fluffy INTERSTITIAL infiltrates involving BOTH lungs typically (not localized in single lobe, not dense infiltrate)

Histological:

  • -Bronchial epithelium loss
  • -Fibrin in lumen
  • -Lymphocytes in bronchial submucosa
  • -Marked interstitial infiltrate (way too many cells in alveolar walls), with clear alveolar spaces
  • -Production of hyaline membranes: where proteinaceous fluid that has exuded into the interstitium coagulates, forms glassy-like substance (looks PINK)
  • -Nodules of lymphocytic infiltration
78
Q

Schistosoma/Schistosomiasis:

What does the infection do to tissues on a physiological level?

A

“Pipestem” fibrosis of liver -> massive fibrous tissue around central veins -> obstruction of portal venous circulation -> portal hypertension, ascites, esophageal varices
–Does NOT destroy hepatocytes: LFTs look normal, normal albumin

Involvement of bladder -> hematuria, squamous cell carcinoma of bladder

79
Q

Schistosoma/Schistosomiasis:

What is the characteristic pattern of cellular response to the infection? What gross and histological changes are seen?

A

Response to egg antigens:

  • -Starts off as cell-mediated Th1 response: febrile disease lasting a few weeks
  • -Develop Th2 type response after several weeks: form granulomas around eggs entrapped in organs

Gross: raised, ulcerated nodules (sites where eggs get through bowel wall)
–Eggs are helped by acute response to transit wall, then get heaped-up nodules from chronic inflammatory response against eggs that don’t get out

80
Q

Entamoeba histolytica:

What does the infection do to tissues?

A

Invasive trophozoites kill PMNs, liquefy tissues, -> “sterile abscess” (can’t grow bacteria from it)

Colitis with “flask-shaped” ulcers:

  • -Ulcer undermines normal colonic mucosa (mucosa lifted up)
  • -Amoebas found in base of ulcer
  • -See abnormal mucosa with lots of bumps
  • -Can penetrate through bowel wall -> peritonitis
81
Q

Entamoeba histolytica:

What is the characteristic pattern of cellular response to the infection? (gross and histological changes)

A

Gross:
Liver abscess with liquefied necrotic material, turns large section of liver white and puss-filled (amoeba at edge of abscess)

Histology:
–Ulcer: Lots of macrophage-like cells (amoebic trophozoites)

82
Q

Pseudomembranous colitis:
What characteristics of the infective agent are important in causing disease?
What does the infection do to tissues?

A

Produces cytotoxins A and B
–Toxin A = the necrotizing agent, destabilizes cellular cytoskeleton -> epithelial cells round up and die

Disease: diarrhea with pseudomembrane formation: fibrin, inflammatory cells, bacteria, and dead host cells
–See C. diff in stool

83
Q

Pseudomembranous colitis:

What is the characteristic pattern of cellular response to the infection? (gross and histological changes)

A

Gross:

  • -Colon can look gray/green and shaggy, OR with white dots
  • -Shaggy material (pseudomembranes) adheres to colonic mucosa

Histological:

  • -Pseudomembrane (mass of fibrin, bacteria, cell debris, inflammatory cells) adherent to mucosa, like a blob sitting on top of the mucosa
  • —Can look like a volcano erupting from small areas of damaged colon and spreading over other parts of the colon
  • -Many normal structures go away
  • -Lots of inflammatory cells present
84
Q

What are examples of pathogens that cause little inflammation? (2)

A 
Cryptococcus neoformans
Plasmodium falciparum (malaria)

Pathology - Quiz 2 (7 decks)

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