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CSB336 > Infectious Diseases > Flashcards

Infectious Diseases Flashcards

1
Q

What is an infectious disease?

A

A disease caused by a microorganism that is potentially transferable to new individuals

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2
Q

What is a communicable disease?

A

An infectious disease that readily spreads from person to person, and is easily caught from an infected person

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3
Q

What are the four types of pathogen?

A

Bacteria, viruses, fungi, and protozoa

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4
Q

Name and describe the two types of immunity

A
  • Nonspecific, innate immunity - composed of highly specialized, systemic cells and processes that eliminate or prevent pathogenic challenges.
  • Specific, acquired immunity - allows for a stronger immune response as well as immunological memory, where each pathogen is “remembered” by a signature antigen
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5
Q

What are the components of innate immunity?

A

External Barriers
• Skin
• Mucous membranes

Chemical barriers
• Chemicals with incidental protective effects
• Antimicrobial proteins (complement and interferons)
• Proteins from naturally occurring bacteria

Cellular defenses
• Scavenger cells (granulocytes, macrophages)
• Natural killer cells

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6
Q

Name two non-specific responses to infection

A

Acute-phase response and inflammatory response

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7
Q

Describe the acute-phase response

A

A group of physiologic changes that occur shortly after the onset of an infection or other inflammatory process and include an increase in the blood level of various proteins, fever, and other metabolic changes.

The end-result of this activation cascade is massive amplification of the response and activation of the cell-killing membrane attack complex.

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8
Q

What is the complement system?

A

The complement system helps or “complements” the ability of antibodies and phagocytic cells to clear pathogens from an organism

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9
Q

Name and describe the basic functions of the complement system

A
  • Opsonisation - enhancing phagocytosis of antigens
  • Chemotaxis - attracting macrophages and neutrophils
  • Lysis - rupturing membranes of foreign cells
  • Clumping of antigen-bearing agents
  • Altering the molecular structure of viruses
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10
Q

True or false: acquired immunity is usually triggered by innate immunity

A

True

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11
Q

What are some components of acquired immunity?

A
  • B and T lymphocytes with specific receptors
  • Central and peripheral lymphoid organs
  • Lymphatic recirculation system
  • Interaction with circulatory, nervous and endocrine systems
  • Products of T and B cells (antibodies, lymphokines)
  • Interactions with the non-specific immune system e.g. antigen presentation
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12
Q

What triggers specific immune responses?

A

Antigens

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13
Q

Describe herd immunity

A

• Above a certain threshold, a condition of ‘herd immunity’ or ‘community immunity’ develops.
• The threshold to achieve herd or community immunity varies by disease and is based on the reproductive and infectious characteristics of the pathogen and the vaccine’s efficacy and duration of protection.
• At that point, it is difficult for a chain of transmission to sustain itself (to the advantage of the public’s health)
• In this way, vaccination offers two forms of benefit:
A) the vaccine recipient becomes personally immune to
infection; and B) the vaccine recipient helps contribute to the collective immunity, making those unable to be
vaccinated less vulnerable to infection.
• Two of the most contagious of the childhood diseases, measles and chickenpox require some of the highest proportions of immunity to achieve herd immunity.

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14
Q

What are the three stages of the infection process?

A
  1. Attachment of the micro-organism to the target cell(s) and, for intracellular pathogens, entry into the host cell
  2. Development of the infection, local multiplication of the pathogen and spread of the micro-organism to distant sites
  3. Shedding of the organism and transfer to a new host.
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15
Q

Fever is defined as…

A

A state of elevated core temperature; it is a regulated rise in core temperature in response to a physiologic threat to the host

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16
Q

Describe the febrile response

A

A cytokine-mediated rise in core temperature, accompanied by increases in acute-phase reactants and a host of other immunologic, endocrinologic, neurologic and physiologic changes.

During the chill or ascending phase of fever, activation of the sympathetic nervous system causes peripheral vasoconstriction and an associated increase in mean arterial pressure.

Oxygen consumption increases, as does carbon dioxide production.

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17
Q

Antipyretic therapy assumes…

A

That fever is, at least in part, noxious and that suppression of fever will eliminate or reduce its noxious effects

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18
Q

What is the definition of bacteraemia?

A

The presences of bacteria in the blood stream

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19
Q

What is the definition of SIRS (systemic inflammatory response syndrome)?

What causes it?

A

A clinical response to a non-specific insult either infectious or non-infectious of origin

Caused by ischemia, inflammation, trauma, or infection. Responses include hyperthermia or hypothermia, tachycardia, tachypnoea, leukocytosis, or leukopenia.

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20
Q

What is the definition of sepsis?

A

Systemic response to infection; defined as the

presence of SIRS in addition to a documented or presumed infection

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21
Q

What is the definition of septic shock?

A

Persistent hypotension and perfusion abnormalities despite adequate fluid resuscitation

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22
Q

What is the definition of MODS (multi-organ dysfunction syndrome)?

A

A state of physiologic derangements in which organ function is not capable of maintaining homeostasis

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23
Q

Describe stage one of SIRS

A

Following an insult, there is local cytokine production with the goal of inciting an inflammatory response thereby promoting wound repair and recruitment of the reticular endothelial system

24
Q

Describe stage two of SIRS

A

Small quantities of local cytokines are released into circulation to improve the local response.

This leads to growth factor stimulation and the recruitment of macrophages and platelets.

This acute phase response is typically well controlled by a decrease in the proinflammatory mediators and by the release of endogenous antagonists; the goal is homeostasis

25
Q

Describe stage three of SIRS

A

If homeostasis is not restored, a significant systemic reaction occurs.

The cytokine release leads to destruction rather than protection.

A consequence of this is the activation of numerous humoral cascades and the activation of the reticular endothelial system and subsequent loss of circulatory integrity.

This leads to end organ dysfunction

26
Q

What are the VSS ranges seen in SIRS?

A

Temperature > 38.3 °C or < 36 °C
HR > 90bpm
RR > 20 or PaCO2 < 32 mmHg

27
Q

What is the definition of sepsis induced hypotension?

A

Presence of a systolic BP <90 mmHg or a reduction of >40 mmHg from baseline in the absence of other causes of hypotension

28
Q

What is the definition of severe sepsis?

A

Presence of SIRS in addition to a documented or presumed infection with associated organ dysfunction, hypoperfusion or hypotension; it is sepsis complicated by organ dysfunction, hypotension before fluid challenge, or lactate ≥ 4 mmol/L

29
Q

Describe the pathophysiology of septic shock

A

Characterized by changes in function of endothelial tissues, in coagulation processes, and in blood flow

Changes appear to be initiated by the cellular release of proinflammatory substances in response to the presence of infectious microorganisms

These interact with the endothelial cells and cause injury to the endothelium and possibly apoptosis of endothelial cells.

Dysregulation of cytokine (small proteins involved in cell signalling) release can lead to endothelial dysfunction characterised by vasodilation and increased capillary permeability

The dysfunctional epithelial barriers enable pathogens and their products to further invade the host organism, disturb regulatory mechanisms, and cause organ dysfunction

Inflammation-induced dysregulation of the
coagulation system, significantly aggravates the
deleterious effects of sepsis and can result in lethal
disseminated intravascular coagulation

30
Q

Septic shock is a hypermetabolic state, and leads to…

A
  • Increased oxygen consumption
  • Global tissue hypoxia
  • Stress hyperglycaemia
  • Major organ dysfunction (hypotension, hypoxia)
31
Q

Septic shock is a combination of…

A

Three classic types of shock:
• Hypovolaemic shock → intravascular fluid losses occurs through capillary leak.
• Cardiogenic shock → myocardial-depressant effects of sepsis.
• Distributive shock → decreased systemic vascular resistance

32
Q

What is warm and cold shock?

A

Warm shockoccurs first and is characterised by high cardiac output and low peripheral vascular resistance (vasodilatation); early septic shock (often reversible)

Most patients will remain in warm shock for 6 to 72 hours before entering cold shock (decreased cardiac output and elevated systemic vascular resistance); refractory septic shock

This late and nearly irreversible phase of septic shock is usually indistinguishable from terminal hypovolemic shock.

33
Q

Describe the events leading to organ failure in sepsis

A

Cardiac function:
• Peripheral vasodilatation leads to an increase in cardiac output.
• Impaired cardiac contractility due to circulating cytokines, nitrous oxide and tumor necrosis factor.

Peripheral vasculature:
• Peripheral vasodilatation which can become refractory.
• Loss of homeostatic regulation of tissue blood flow.
• Shunting of blood through capillary beds → hypoxia.
• Leads to metabolic acidosis.

Renal failure:
• Impairment of renal microvasculature → reduction in renal perfusion and glomerular filtration → acute tubular necrosis.

Respiratory failure:
• Development of acute respiratory distress syndrome.
• Neutrophils cause damage to the endothelium and subsequent degranulation of lung leads to accumulation of fluid and inflammatory cells in lungs.
• This leads to impaired gas exchange → hypoxia.
• Increased pulmonary vascular resistance in contrast to the fall in systemic vascular resistance → interstitial oedema and pulmonary hypertension.

34
Q

Outline the sepsis criteria

A

Infection confirmed or suspected plus:
• Temperature > 38.3C or < 36C (normal temperature does not exclude sepsis)
• Respiratory rate > 20 / minute
• Heart rate > 90/minute
• Acute confusion or decreased level of consciousness
• Hyperglycaemia (blood glucose > 7.7 mmol/L in patient without diabetes)
• Oliguria (urine output less than 0.5 mL/kg/hour)

35
Q

Outline the septic shock criteria

A 
Infection confirmed or suspected plus:
• Mottled or cold peripheries
• Capillary refill time > 3 seconds
• Systolic BP < 90 mmHg or MAP < 60 mmHg
• Purpuric rash
• Arterial or venous lactate > 2 mmol/L
• Oliguria (urine output less than 0.5 mL/kg/hour)
36
Q

What are the four points of early goal directed therapy (EGDT)?

A

Early identification
Early oxygenation
Early haemodynamic resuscitation
Hospital notification

37
Q

What is meningitis?

A

Inflammation of the protective membranes covering the brain and spinal cord known collectively as the meninges

The inflammation may be caused by infection of viruses, bacteria, or other microorganisms, and less commonly by certain drugs (NSAID’s, antimicrobials)

38
Q

What are the symptoms of meningitis?

A
  • Neck stiffness
  • Headache
  • Fever
  • Photophobia
  • Phonophobia
  • Altered mental status
  • Irritability
  • Nuchal rigidity
  • Positive Kerning’s sign (extension of leg while hip is still flexed causes pain and hamstring muscle spasm) and/or Brudzinski’s sign (automatic flexing of hips and knees when examiner flexes pt’s neck when they are supine)
39
Q

What is the causative agent of meningococcal disease?

A

Neisseria meningitidis

40
Q

What is the transmission mechanism of meningococcal disease?

A

Respiratory droplets

41
Q

True or false: meningococcal disease can present as septicaemia, meningitis, or both

A

True

42
Q

Describe the pathophysiology of meningococcal disease

A

Tissues damage is most often caused by host immune mechanisms activated by endotoxin

Endotoxin binds to plasma endotoxin binding protein and to the cellular receptor triggering and intense inflammatory response

Activated macrophages produce a range of proinflammatory cytokines

Microvascular injury manifests as increased vascular permeability leading to proteinuria and hypovolemia, vasoconstriction or vasodilation, intravascular thrombosis and myocardial dysfunction

43
Q

Describe the clinical presentation of meningococcal disease

A
  • Flu-like symptoms
  • Fever not responsive to antipyretics
  • Hypotension
  • Tachycardia
  • Cool/cold skin and/or delayed capillary refill
  • Pale or blotchy complexion
  • Confusion or delirium
  • Seizures
  • Tachypnoea
  • Decreased conscious level
  • Neck pain or stiffness
  • Photophobia
  • Headache
  • Diarrhoea
  • Nausea and/or vomiting
  • Inability to walk/weakness
  • Rigors
  • Body aches and pains
  • Weakness/lethargy
  • Rash (may be petechial, purpuric (80%) or maculopapular (13%); generally non-blanching; may blanch in early stages of the disease; may be no rash at all (up to 7% of cases); rapidly developing rash is generally associated with poor prognosis)
44
Q

What drug is used in the mx of meningococcal disease?

A

Ceftriaxone

45
Q

What is encephalitis?

A

Inflammation of the brain.

  • Can be present as the direct effects of a viral or bacterial infection or as a secondary sequelae.
  • Certain parasitic or protozoal infestations can also be responsible; herpes is a common viral cause.
46
Q

What are the symptoms of encephalitis?

A
  • Fever
  • Headache and hhotophobia
  • Weakness
  • Seizures
  • Less commonly: nuchal rigidity, stiffness of the limbs, slowness in movement and clumsiness (depending on which part of the brain is involved)
47
Q

Describe hepatitis

A

Hepatitis means inflammation (swelling and pain) of the
liver - it may be caused by infection, viruses, chemicals, alcohol, drug use and other factors.

The various forms of viral hepatitis include hepatitis A,
B, C, D and E (Hepatitis D and E are uncommon in Australia)

‘Chronic hepatitis’ means ongoing inflammation of the
liver, irrespective of the underlying cause

48
Q

Summarise hepatitis A

A

Hepatitis A
• Can be infected by direct contact with the hepatitis A virus through food, drinks or objects contaminated by the faeces of an infected person.
• Symptoms may last several weeks but the person usually recovers completely.
• Infection with hepatitis A will give lifelong immunity.
• Short term vaccination available

49
Q

Summarise hepatitis B

A
  • Hepatitis B virus is found in the blood and, to a lesser degree, in body fluids such as semen and vaginal secretions.
  • Vaccination is available
50
Q

Summarise hepatitis C

A
  • Hepatitis C is a blood-borne virus that is spread when blood from an infected person enters another person’s bloodstream.
  • In Australia, the most common way it is transmitted is through sharing unsterile injecting drug equipment.
  • Around 20 to 30 per cent of people who have been infected with hepatitis C may clear the virus from their blood with no treatment.
  • Around 70 to 80 per cent of people infected with hepatitis C, if untreated, may continue to have the virus in their blood and are likely to have chronic hepatitis C.
  • Of these, about 10 to 20 per cent will develop cirrhosis, which is scarring of the liver. This can take 20 years or more to develop.
51
Q

What are the symptoms of hepatitis?

A
  • Not everyone with hepatitis has symptoms.
  • When symptoms occur, they may include:
  • Fever
  • Nausea
  • Abdominal discomfort
  • Dark urine
  • Lethargy
  • Painful joints
  • Oedema
  • Easy bruising
  • Jaundice
52
Q

What is measles?

A

Measles is transmitted by aerosolised particles from the respiratory secretions of infected individuals directly to susceptible hosts.

  • The particles can also persist in the environment for more than 1 hour and be acquired by inhalation.
  • Individuals with measles are most infectious during the prodromal stage (which occurs 7 to 10 days after exposure) through the fourth day after the onset of rash.
  • Measles is highly contagious, and symptomatic infection develops in virtually all susceptible exposed individuals.
53
Q

Differentiate between HIV and AIDS

A

Human Immunodeficiency Virus (HIV), of which there are retrovirus strains (HIV-1 or HIV-2), that attacks the T-cells of the immune system with debilitating effects, producing a syndrome called acquired immune deficiency syndrome (AIDS).

• AIDS is a disease caused by HIV and characterized by profound immunosuppression that leads to opportunistic infections, secondary neoplasms, and neurologic manifestations.

54
Q

What is neutropenia?

A
  • An abnormally low concentration of neutrophils
  • Patients with neutropenia are more susceptible to bacterial infections and, without prompt medical attention, the condition may become life-threatening
  • Microbial invasion and development of infection are facilitated by the presence of co-morbidities, immunosuppression and damage to anatomic barriers caused by the cancer itself or induced by chemotherapy or invasive procedures
  • Obstruction of the lumen of natural body passages (i.e. urinary, biliary, respiratory or digestive tract) by cancer impairs the flow of body fluids and secretions, creating conditions that promote microbial growth.
  • Cytotoxic chemotherapy damages the epithelial tissue lining, resulting in loss of the integrity of the mucous membrane barrier.
  • Development of mucositis therefore predisposes to infection by the patient’s endogenous commensal flora and colonizing pathogens.
  • Injury to the skin by venous puncture, presence of indwelling vascular access devices, bone marrow aspiration, lumbar puncture and other surgical interventions can also promote skin and soft tissue infections.

Common toxicity of chemotherapy.
• More at risk if combined with radiotherapy.
• Occurs with chemotherapy agents that have a myelosuppressive effect on the bone marrow.
• Reduces white blood cells mainly neutrophils.
• If on high dose steroids may “blunt” inflammation response
• Febrile neutropenia is a true medical emergency (leads quickly to sepsis → death)
• Consider in all patients receiving or have recently received chemotherapy (cytotoxic)
• Remember the patient will be immuno-suppressed so particular attention to universal precautions and infection control.

55
Q

Discuss UTIs in elderly pts

A
  • One of the most common infections in the elderly.
  • May present atypically such as malaise, anorexia, weakness and subtle mental status changes.
  • Typical presentations include urinary frequency, incontinence, dysuria, fever, and flank pain.

CSB336 (14 decks)

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