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Infectious Diseases Flashcards

1
Q

Describe the virulence factors of Staph aureus. What infections do the different species of Staph aureus cause?

A
  1. Staph aureus causes disease by
    - Producing exotoxins causing host damage
    + Alpha toxin: Membrane depolarization/damage
    + Beta toxin: Sphingomyelinase
    + Superantigens: Toxic shock syndrome (TSS), food poisoning
    - Surface proteins to adhere to host endothelium cell -> Allows evasion from immune system
    - Secretes enzymes that degrades proteins -> Allows formation of abscess
  2. Types of infection cause by staph
    - Staph aureus: Skin, pneumonia, osteomyelitis
    - Staph epidermidis: IE in prosthetic valves
    - Staph saprophyticus: UTI
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2
Q

What are the risk factors for Toxic Shock Syndrome? What are the clinical features for Toxic Shock Syndrome?

A
  1. Risk factors for TSS
    - Use of tampon
    - Nasal packing
    - Post-op wound infection
    - Staph or strep skin infection
  2. Clinical features of TSS
    - Hypotension
    - Acute renal failure
    - Respiratory failure
    - Coagulopathy
    - Fever
    - Soft tissue necrosis at site of infection
    - Generalized erythematous rash
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3
Q

Name some common bacteria that causes wound infection. What diseases are caused by Staph aureus?

A
  1. Bacteria causing wound infections
    - Staph aureus
    - Strep pyogenes
    - Pseudomonas aeruginosa
    - Clostridium perfringes
    - Clostridium tetani
  2. Diseases caused by Staph aureus
    - Skin infections: Cellulitis, impetigo, abscess, scalded skin syndrome
    - Osteomyelitis
    - Endocarditis
    - Pneumonia
    - Food poisoning
    - Toxic shock syndrome
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4
Q

Describe the structure of the influenza virus. What are the types and subtypes? What is the pathological basis of epidemics and pandemics?

A
  1. Structure of influenza virus
    - Single stranded RNA (ssRNA) virus
    - Bounded by nucleoproteins which determines its type (A, B, C)
    - Spherical capsule
    - Lipid bilayer containing haemaglutinin (H) and neuraminidase (N) which determines its subtype
  2. Types and subtypes
    - Types: A, B, C determined by nucleoproteins
    - Subtypes: Haemaglutinins, neuraminidase
  3. Epidemics and pandemics caused by Influenza A. Not usually seen with Influenza B or C
    - Epidemics are caused by antigenic DRIFT -> Mutation in H + N to allow virus to evade immune system
    - Pandemics are caused by antigenic SHIFT -> Change in H + N by recombinant RNA from animal virus
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5
Q

How does the human body clear a primary influenza virus infection? How does influenza virus causes pneumonia?

A
  1. Influenza virus cleared via 2 mechanisms
    - Cytotoxic T cells -> Attacks cells infected by virus
    - Macrophages producing anti-influenza proteins
  2. Influenza virus causes pneumonia by
    - Virus first attach to upper respiratory tract epithelium
    - Causes necrosis of cells
    - Triggers inflammation
    - Interstitial inflammation in alveoli
    - Secondary infection by strep/staph
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6
Q

What are streptococci? Name some different types of streptococci and examples of diseases they cause. What factors in streptococci contribute to their virulence? What are some post-infectious syndromes caused by streptococci?

A
  1. Streptococci are
    - Gram +ve cocci in pairs or chains
    - Obligate anaerobes
    - Cause suppurative infections and post-strep syndromes
  2. Types of streptococci and disease
    - Alpha hemolytic
    + Strep pneumonia - Pneumonia, meningitis
    + Strep viridans - Infectious endocarditis
    - Beta hemolytic
    + Group A (Strep pyogenes) - Pharyngitis, rheumatic fever, impetigo, scarlet fever, post-strep glomerulonephritis
    + Group B (Strep agalactiae) - Chorioamnionitis, neonatal sepsis
    - Strep mutans - Dental caries
  3. Streptococci virulence
    - Pyrogenic exotoxins -> Fever and rash
    - Capsule -> Prevents phagocytosis
    - M proteins -> Inhibits complement cascade activation
    - Pneumolysins -> Damage to cell host membrane
  4. Post-streptococci infectious syndromes
    - Rheumatic fever
    - Post-strep/Immune mediated glomerulonephritis
    - Erythema nodosum
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7
Q

What is croup?

A
  1. Croup is acute laryngotracheobronchitis
    - Acute inflammation, edema and narrowing of the upper airway
    - Usually caused by viruses -> Parainfluenza, RSV, adenovirus
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8
Q

What type of organisms are Clostridia? Name the organisms and diseases they cause in humans. How does botulism toxin cause disease? What is the pathogenesis of gas gangrene?

A
  1. Clostridia is
    - Gram +ve bacilli
    - Anaerobic
    - Spore-forming bacteria
  2. Disease caused
    - Clostridium difficile -> Pseudomembranous colitis
    - Clostridium perfringens -> Gas gangrene
    - Clostridium botulinum -> Flaccid paralysis
    - Clostridium tetani -> Tetani
  3. Botulism toxin
    - Usually ingested in contaminated food
    - A particle which cleaves synactobrevin required to fuse neurotransmitter vesicles
    - Causes flaccid paralysis
  4. Pathogenesis of gas gangrene
    - Caused by clostridium perfringes or septicum
    - Produces a-toxins -> Phospholipases C and destructs membrane, muscles, RBC
    - Releases enzymes -> Collagenase, hyaluronidase -> Causes membrane damage
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9
Q

What is the clinical spectrum of Candida infection? What mechanisms enable Candida to cause disease?

A
  1. Clinical spectrum of Candida infection
    - Benign commensal
    - Superficial mucosal infection -> Candidiasis -> Mouth, esophagus, vagina
    - Superficial cutaneous infection -> Nappy rash, folliculitis
    - Widespread invasive disease -> Bacteraemia, endocarditis, myocarditis, meningitis
  2. Virulence factor of Candida
    - Adhesion to host cells
    - Phenotypic switching
    - Production of enzymes that degrades ECM
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10
Q

Which bacteria class does E.coli belong to? What is the difference between endotoxins and exotoxins? List some types of infection commonly caused by E.coli.

A
  1. E.coli
    - Gram -ve rod
    - Anaerobic bacteria
  2. Exotoxins vs endotoxins
    - Exotoxins: Lipopolysaccharide found on cell wall of Gram -ve bacteria -> Triggers the immune response causing injury to cells
    - Endotoxins: Proteins secreted by bacterial -> Causes direct injury to cells
  3. Infection caused by E.coli
    - UTI
    - Prostatitis
    - Epididymo-or Haiti’s
    - Infectious Enterococci this
    - Cholecystitis
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11
Q

Describe the pathogenesis of glandular fever. What are the clinical features of glandular fever? What are the outcomes of glandular fever?

A
  1. Pathogenesis of glandular fever
    - Caused by Epstein-Barr virus (EBV)
    - Transmitted via droplets and close contact -> Saliva
    - Infects lymphoid tissues -> Tonsils first
    - Triggers B cells and T cells response
    - B cells -> Lysis of infected tissue and involved in latent infection
    - T cells -> Produces immune response and appears with onset of symptoms
    - IgM and IgG antibodies produced
    - Infection resolves typically after 4 - 6 weeks
  2. Clinical features of glandular fever
    - Fever
    - Sorethroat
    - Lymphadenopathy
    - Myalgia
    - Arthralgia
    - Hepatitis
    - Abdominal pain
    - Lethargy
  3. Outcomes
    - Resolves within 4 - 6 weeks
    - Hepatitis
    - Splenic rupture
    - Lymphoma
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12
Q

Please give some examples of Herpes simplex infection. After primary herpes simplex infection, how does reactivation occurs?

A
  1. Examples of Herpes simplex infection
    - Cold sores
    - Genital herpes
    - HSV encephalitis
    - Keratitis
  2. Reactivation of herpes simplex infection
    - After primary infection, virus hides in nucleus of sensory neurone (dorsal root ganglion)
    - Remains inactive and replicates by producing viral mRNA only to avoid detection by immune system
    - Reactivates during period of immunocompromised by avoiding immune recognition
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13
Q

Describe the pathogenesis of Herpes zoster infection

A
  1. Pathogenesis of Herpes zoster infection
    - Begins with primary infection -> Previous exposure by chickenpox or subclinical disease
    - Hides in nucleus of sensory neurone (Dorsal root ganglia)
    - Remains latent/dormant for many years
    - Reactivated during period of immunocompromised/elderly
    - Vesicular eruptions along dermatomes of sensory nerves
    - Can be complicated by VZV ophthalmicus, Ramsay-Hunt syndrome
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14
Q

What are the major pathological sequelae of HIV infection? What are the modes of transmission of HIV?

A
  1. Pathological sequelae of HIV infection
    - Infected by HIV virus
    - Replicates
    - Attacks CD4+ T lymphocytes
    - Causes profound immunosuppression
    - Risk of opportunistic infection and neoplasm
  2. Modes of transmission of HIV
    - Vertical: Mother-to-baby
    - Parenteral: IVDU, contaminated blood products, needlestick injury
    - Body fluids: Sexual partners
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15
Q

What organism causes malaria? Describe the pathogenesis of Malaria. How does P.falciparum present clinically? How does P.falciparum differ from other forms of malaria? What factors can make people less susceptible to malaria?

A
  1. Malaria caused by parasitic protozoa
    - Plasmodium falciparum
    - Plasmodium vivax
    - Plasmodium ovale
    - Plasmodium malariae
  2. Pathogenesis of malaria
    - Transmitted by mosquitoes
    - Plasmodium injected into blood stream
    - Travels to liver and invades hepatocytes
    - Multiplies in hepatocytes until it ruptures
    - Released into the blood stream and binds to RBC
    - Replicates in vacuoles on RBC until it ruptures again
    - Further invades other RBC
  3. Clinical presentation of malaria
    - Fever could be cyclical
    - Lethargy
    - Malaise
    - Anaemia
    - Hepatomegaly
    - Splenomegaly
    - Bleeding disorders -> Mucosal, urine
    - DIC
    - Acute pulmonary edema
    - Cerebral symptoms
  4. P.falciparum vs other types of malaria
    - P.falciparum infects all types of RBC -> Clumping of RBC -> Higher levels of parasites
  5. Reduce susceptibility to malaria by
    - Sickle cell anaemia
    - Repeated exposure stimulates immune response
    - Malaria prophylaxis
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16
Q

What type of virus is Measles? How is it spread? Describe some of the clinical manifestations of measles infection. What immune response occur as a result of Measles infection? Describe the pathogenesis of measles infection

A
  1. Measles virus
    - Single-stranded RNA virus
    - Paramyxovirus family
  2. Measles spread via respiratory droplets
  3. Clinical manifestations of measles
    - Fever
    - Rash
    - Koplik spots (oral mucosal ulceration)
    - Cough/coryza
    - Acute measles encephalitis
    - Viral pneumonia
    - Conjunctivitis
    - Croup
  4. Immune response
    - Triggers T-lymphocytes -> Produce antibodies -> Controls infection -> Causes rash
  5. Pathogenesis of measles infection
    - Caused by measles virus -> Single stranded RNA virus of paramyxovirus family
    - Transmitted via respiratory droplets
    - Attaches to upper respiratory tract mucosal and replicates in epithelial cells
    - Hematogenous spread
    - Preventable with vaccine
17
Q

How does Neisseria meningitidis cause infection? What are the clinical consequences of Neisseria meningitidis infection? Apart from Neisseria, what else can cause meningitis? What are the microbiological features of Neisseria? What are the clinically significant Neisseria?

A
  1. Pathogenesis of Neisseria
    - Common commensal
    - Healthy individuals mount immune response to clear infection
    - Causes invasive disease when exposed to different serotype
    - Spreads via respiratory droplet
    - Invades upper respiratory tract epithelium
    - Goes into blood stream
    - Causes widespread infection
    - Has capsule which allows evasion from immune system -> Avoids opsonisation and complement destruction
  2. Clinical consequences of Neisseria infection
    - Meningitis
    - Encephalitis
    - Seizures
    - Sensorineural hearing loss
    - SIADH
    - Hydrocephalus
    - Septicaemia
    - Death
  3. Organisms causing meningitis
    - Bacteria: E.coli, haemophilus influenzae, strep pneumoniae, enterococcus
    - Viral: Enterovirus, measles
    - TB
    - Autoimmune
  4. Microbiological features of Neisseria
    - Gram -ve diplococci
    - Aerobic bacteria
    - Stains with chocolate agar
  5. Neisseria infections
    - Neisseria meningitidis -> Meningitis
    - Neisseria gonorrhea -> STI
18
Q

What are the 2 clinical conditions caused by Varicella Zoster virus? Describe the pathogenesis and clinical course of infection with this virus. What are the complications of chicken pox? What tissues may be involved in a primary Varicella Zoster infection? What is shingles?

A
  1. Clinical conditions caused by Varicella Zoster
    - Chicken pox
    - Shingles
  2. Pathogenesis of infection with Varicella Zoster
    - Infection by varicella zoster virus transmitted via aerosol or direct contact spread
    - Causes primary infection -> Chicken pox
    - Widespread vesicular lesion -> Crusts up
    - Virus hides in nucleus of sensory neurone (dorsal root ganglia)
    - Lays dormant/inactive for many years
    - Reactivate in later years or immunocompromised states
    - Causes shingles in reactivation with vesicular lesion spreading along dermatomes area of nerve
  3. Complications of chicken pox
    - Interstitial pneumonia
    - Skin infection
    - Shingles
    - Encephalitis
  4. Tissue involved in primary VZV infection
    - Skin
    - Mucous membrane
    - Nerves
  5. Shingles
    - Reactivation of the varicella zoster virus which lays dormant in the dorsal nerve root
    - Presents as vesicular lesion along dermatome supplied by nerve
    - Can lead to interstitial pneumonia, encephalitis, visceral lesions

Pathology (17 decks)

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