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NURS 1650 - Here We Go Again > Pathophysiology of Bacterial Infections: Pneumonia, UTI, and IE > Flashcards

Pathophysiology of Bacterial Infections: Pneumonia, UTI, and IE Flashcards

1
Q

What are the most common infection sites?

A

Respiratory tract

Urinary tract

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2
Q

What is virulence?

A

The strength of a microorganism’s pathogenicity

Virulence factors: adhesins, protective capsules

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3
Q

What is inoculum?

A

The quantity of microorganisms

“How many microorganisms cause ___?”

ex. COVID, the inoculum is higher in an enclosed space rather than outside

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4
Q

The chain of transmission of an infection

A

Infectious agent

Reservoir

Portal of exit

Mode of transmission

Portal of entry

Susceptible victim

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5
Q

What is a nosocomial infection?

A

An infection acquired during the course of a stay in a hospital, nursing home, or other healthcare facilities

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6
Q

What are the stages of infection? Describe each one

A

Incubation: between exposure and symptoms

Prodrome: non-specific symptoms

Illness: overt s/sx of infection

Recovery: return toward homeostasis

Chronic Carrier State: is possible in some infections

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7
Q

What is community-acquired pneumonia (CAP)?

A

Acquired outside of hospitals or extended-care facilites

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8
Q

What is hospital-acquired pneumonia (HAP)?

A

Acquired in the hospital

> 48 hours after admission

Increased risk for MDR (multi-drug resistant) bacteria

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9
Q

What is ventilator-associated (VAP)?

A

Diagnosis made 48-72 hours after endotracheal intubation

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10
Q

What is healthcare-associated (HCAP)?

A

Diagnosis made while in the community or < 48 hours after hospital admission

Usually following ICU admission

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11
Q

What is the most common pathogen in all types of locations?

A

Streptococcus pneumonia

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12
Q

What are some risk factors for pneumonia?

A

Young and old people

Smoker

Lung disease

Dysphagia

Immobility and/or depressed cough reflex

IVDU

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13
Q

What is pneumonitis?

A

Pneumonia caused by a chemical source

Inhalation of liquid, gases, or small particles

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14
Q

What is atypical pneumonia? How is it presented?

A

Pneumonia with different symptoms than typical pneumonia

Appear different on x-ray

Respond to different antibiotics

Extrapulmonary s/sx: confusion/change in mental status, GI symptoms, ear pain, sore throat

DOES not mean it is uncommon

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15
Q

What is walking pneumonia?

A

Patient will look fine and healthy but have pneumonia

no s/sx

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16
Q

Name the normal respiratory tract defense mechanisms

A

Cilia

Mucus

Mucociliary Escalator

Cough Reflex/ Swallowing

Alveolar Macrophages

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17
Q

What virulence factors does S. pneumoniae have?

A
  • Able to avoid phagocytosis
  • Secretes a protein that permits it to adhere to the mucosa
  • Secretes a protein that lyses and destroys ciliated cells
  • Secretes a protease that inhibits the function of IgA
  • Secretes hydrogen peroxide –> damage to host cells
  • Activates inflammatory cascade
  • Induces vascular permeability
  • May become invasive –> move into blood or BBB
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18
Q

How does S. pneumoniae avoid phagocytosis?

A

Its external polysaccharide capsule prevents opsonization by complement

** Most important virulence factor

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19
Q

What does IgA do? How does S. pneumoniae affect it?

A

IgA normally binds bacteria to mucus to facilitate clearance from the respiratory tract

S. pneumoniae secretes a protease that inhibits function of secretory IgA

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20
Q

How does bacteria make its way to the lungs?

A

Inhalation (nose)

Aspiration (mouth)

Hematogenous (bloodstream)

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21
Q

Which patients are we going to be most concerned about, regarding their risk for aspiration?

A

Patients with dysphagia (ex stroke patients)

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22
Q

What are neutrophil extracellular traps (NETS? What do they do?

A

A meshwork containing antimicrobial proteins that trap and kill bacteria

Extruded by neutrophils

Can also cause damage

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23
Q

What happens when alveolar air spaces fill with exudative fluid and debris?

A

Decreased gas exchange

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24
Q

What causes the clinical manifestations of pneumonia?

A

The inflammatory response rather than the proliferation of the bacteria

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25
Q

S/Sx of Pneumonia

A

Fever

Chills

Dyspnea

Productive cough

Pleuritic chest pain

Tachycardia

Diminished breath sounds

Inspiratory crackles

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26
Q

Definition of a UTI

A

Significant bacteria anywhere along the urinary tract, from the kidneys to the urethra

27
Q

UTIs are more frequent in people born with ____ urethras

A

Shorter urethras

28
Q

Lower UTI vs Upper UTI

A

Lower UTI:
- Cystitis
- Infection confined to the bladder and/or urethra

Upper UTI:
- Pyelonephritis
- Infection is above the bladder (i.e., kidneys, ureters, peri-renal tissue)

29
Q

What is vesicoureteral reflux? What can it result in?

A

Condition in which the ureterovesical junction (UVJ) fails to function as a one-way valve, allowing urine and bacteria to reflux back to the kidney

Causes urine and bacteria to reflux back into the kidney

Chronic infection can cause scarring in the kidney

30
Q

Complicated vs. Uncomplicated UTI

A

Complicated:
- associated with an underlying condition that increases the risk of therapy failure (ex. DM, pregnancy, renal failure, presence of a catheter)

Uncomplicated:
- Healthy, nonpregnant adults with no risk factors for treatment failures

31
Q

Name the normal defenses mechanisms of the urinary tract

A

Urination – flushes out bacteria before it adheres

Low bladder pH

Proteins secreted by kidneys prevent bacterial adherence

Vaginal lactobacilli kill uropathogens

Prostatic secretions are also bactericidal

Secretory IgA

The mucopolysaccharide lining of the urethra/bladder makes it difficult for bacteria to penetrate and adhere

Cell apoptosis –> exfoliate/desquamate –> bacteria are carried away in urine

Inflammatory response by neutrophils and cytokine signaling

32
Q

Why is E. coli such a common cause of UTI?

A
  • Present in large amounts in the lower gut (close to the vagina and urethra)
  • Its flagella permit motility
  • Virulence factors (adhesins, fimbriae, capsule, inflammation, hemolysin, toxins, iron transport system)
33
Q

What are E. coli’s virulence factors? Describe each one

A

Adhesins allow binding and attach to the urethra and bladder

Fimbriae permit adherence to uroepithelial cells and also block phagocytosis

Polysaccharide capsule prevents phagocytosis and complement attachment

Induces inflammation and exfoliation –> tissue damage –> easier for bacteria to invade

Hemolysin production: induces the formation of pores –> cell lysis

Iron transport system –> uptake iron even in iron-poor environments

Produce toxins

34
Q

How does E. coli avoid phagocytosis?

A

Its fimbriae permit adherence to the uroepithelial cells and block phagocytosis

Its polysaccharide capsule prevents phagocytosis

35
Q

How does a lower UTI occur? Describe the steps

A
  1. Bacteria ascend the urethra
  2. Attach to the bladder epithelium
  3. Invade the epithelium
  4. Replicate (produce a biofilm)
  5. Bacterial toxins and proteases cause exfoliation of cells
  6. Inflammatory response to the invasion, the possibility of bacterial persistence in the epithelium

Can continue to ascent to the ureter to the kidneys (pathway to pyelonephritis)

36
Q

How does a lower UTI progress to pyelonephritis (upper UTI)? What can this then lead to?

A

Bacteria continue their ascension up the urethra and into the kidney(s)

Can lead to acute kidney injury (AKI)

37
Q

Lower UTI s/sx

A
  • Dysuria
  • Urgency
  • Frequency
  • Nocturia
  • Suprapubic heaviness or pain
  • Gross hematuria (see blood in urine)
38
Q

What would you see in the labs of a person with a lower UTI?

A

Bacteriuria

Pyuria (WBC)

Nitrite

Leukocyte esterase

39
Q

How do the presence/absence of nitrites and leukocyte esterase affect a UTI diagnosis?

A

The absence of nitrites or leukocyte esterase does not necessarily rule out a UTI

Their presence provides enough evidence that a UTI is likely occurring

40
Q

Upper UTI s/sx

A
  • Fever, chills
  • Flank pain
  • Nausea/vomiting
  • Malaise

Can be with or without lower UTI s/sx

41
Q

Upper UTI CVA PE:

A

Costovertebral tenderness present

42
Q

What would you expect to see in the labs of a person with an upper UTI?

A

Bacteriuria

Pyuria (WBC in urine)

Increased serum WBCs

Nitrite

Leukocyte esterase

43
Q

How are UTIs clinically presented in pediatric patients?

A

Infants and children under 2 y.o. may present with FEVER as the sole manifestation of UTI

Children above 2 y.o. will often have the same sx as an adult, but will complain of abdominal pain and bladder incontinence

44
Q

How are pneumonia and UTI clinically presented in geriatric patients?

A

They may not present with any of the classic symptoms. They may not even be febrile

A common cluster of s/sx of both pneumonia and UTI in a geriatric patient is a “change in mental status”:
- Confusion
- Delirium
- Lethargy
- Sudden incontinence in a previously continent patient

45
Q

Delirium vs. Dementia

A

Delirium:
- Sudden onset
- Dramatic changes in cognition in behavior (morning vs. night)
- Can vary/have periods
- Reversible
- Can be brought on by infection, pain, other illness, disorientation of the hospital setting

Dementia:
- Develop over the years
- Progressive changes in cognition and behavior
- Will not vary in the course of a single day
- Not reversible

46
Q

What is asymptomatic bacteriuria? What does this mean for our geriatric patients? What problems can arise?

A

A patient with a significant bacterial count in the urine, but the patient has no dysuria, increased frequency, fever, etc.

IDSA 2019 guidelines do not recommend screening and treating older adults with delirium / asymptomatic bacteriuria to avoid ADE such as C. diff infections.

It creates a fine line to balance the risk of infection –> sepsis with the risk of inappropriate drug treatment –> ADE

We don’t not want to treat an infection bc it can lead to sepsis but we also do not want to cause ADE/resistance.

47
Q

Are there any exceptions to the “do not screen rule”?

A

Yes

Pregnant people due to a high risk of progression of symptomatic upper/lower UTI

Patients who undergo a urological procedure in which mucosal trauma is expected

48
Q

What is the endocardium? What does it do?

A

thin, smooth layer that lines the chambers of the heart and also covers the valves

Its surface normally inhibits platelets, RBCs, and transient bacteria from attaching

49
Q

What is ineffective endocarditis (IE)?

A

An infection of the endocardium, usually of the endocardium covering valves

50
Q

What is a cardinal feature of IE?

A

Growth of “vegetation” on infected surfaces

Vegetations: dense aggregate of platelets, fibrin, pro-inflammatory, WBCs, bacteria, and other substances such as collagen

Tends to shield bacteria from the normal innate immune process

51
Q

What are some causative microbes of IE?

A

S. aureus (most common)

Streptococci

Enterococci

Fungal (rare, but difficult to treat)

52
Q

What contributes to vegetation finding a place to attach and grow in IE?

A

Structural heart disease –> surface that promotes attachment

Certain Gram+ bacteria, such as S. aureus, are able to release substances that allow them to attach even to smooth endocardium

53
Q

What causes damage to the endocardium in IE?

A

IVDU practices thought to cause endocardial surface damage

Injection of cocaine –> vasospasm –> tissue damage

Damage to endocardium –> platelet-fibrin thrombus complex deposited on the surface –> thrombus grows larger along with vegetation making it difficult for antibiotics to kill bacteria

Bacteria also induce an inflammatory response –> more tissue damage

Vegetations may disseminate –> break off and enter circulation –> leading to stroke or MI

54
Q

Clinical presentation of IE:

A

Non specific fever

Pneumonia, pleural effusion, empyemia (pus collection in pleural space)

May present with stroke, kidney failure or infarct of other organ systems

May already be in sepsis

Heart mummurs in non-IVDU

55
Q

What must be present to diagnose IE?

A

Blood cultures x 3 showing microorganisms consistent with IE

Echocardiogram showing vegetation, abscess, or new partial dehiscence of prosthetic valve

Have a high index of clinical suspicion for anyone who has risk factors for IE and presents acutely ill

56
Q

What are some sequelae of IE? What causes them?

A

Destruction of affected cardiac valve(s) and other tissue –> acute heart failure

Bits of vegetation may break off and embolize
- Stroke
- MI
- Pulmonary embolism
- Kidney failure
- Infarct necrosis of extremities

57
Q

What is bacteremia? How does it occur?

A

Bacteria in the bloodstream

Results from translocation of bacteria from tissue or introduction by a break in skin/mucosal defenses

Potential sequelae of infection

58
Q

What is sepsis?

A

Life-threatening organ dysfunction caused by the dysregulated host response to infection

Inappropriate, widespread inflammation is usually the culprit

59
Q

S/Sx of Sepsis

A

Hypotension

Shivering, feeling cold

Fever

Extreme pain or discomfort

Diaphoresis or clammy skin

Confusion or disorientation

SOB, tachycardia, hypotension, low O2 stat

Organ failure

60
Q

What is septic shock?

A

Defined as sepsis in which particularly profound circulatory, cellular, and metabolic abnormalities are associated with a greater risk of mortality than sepsis alone

61
Q

What are the two markers of septic shock?

A
  1. Persistent hypotension that requires vasopressors to maintain MAP > 65 mm Hg
  2. Serum lactate level > 2 mmol/L despite adequate volume resuscitation

May result in circulatory failure

62
Q

What does the initial, rapid treatment of sepsis include?

A

Labs: measurement of serum lactate, blood cultures before Abx are started

Measures to increase MAP (fluids, vasopressors)

Early, broad-spectrum Abx until a culprit pathogen is identified –> de-escalate or change antimicrobial

63
Q

What are some lingering effects of sepsis?

A

Muscle weakness

Fatigue

Difficulty swallowing, concentrating, sleeping

Anxiety, sadness, poor memory

64
Q

What are the top two infections that lead to sepsis?

A

Pneumonia and UTI

NURS 1650 - Here We Go Again (20 decks)

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