Chap 8- Infectious diseases Flashcards
types of physical barriers
- skin defenses
- GI tract defenses
- respiratory tract defenses
- urogenital tract defenses
skin barriers
- keratinized outer layer
- low pH
- fatty acids
GI tract defenses
- gastric acid
- pancreatic enzymes
- bile detergents
- peyer patches
- defensins
- peristalsis
- protective flora
respiratory tract defenses
- bronchial epithelium ciliary activity
- mucous layer
- defensins
- IgA
- alveolar macrophages
urogenital tract defenses
- frequent bladder flushing with urine
- low vaginal pH
- intact epidermal/ epithelial barrier
what factors influence consequences of infectious disease?
- virulence of organism
- magnitude of infection
- pattern of seeding
- host factorts
how are most pathogens transmitted?
- respiratory
- fecal oral
- sexual
stages of infection
- host encounter
- gain entry
- multiply and spread
- direct or indirect tissue inury
what are possible outcomes of infection
- resolution
- chronic active infection
- prolonged asymptomatic excretion of agent
- latency
- host death
what are some mechanisms of immune evasion?
- antigenic variation
- resistance to antimicrobial peptides
- resistance to phagocytes
- evasion of apoptosis and maniupation of host cell metabolism
- resistance to cytokine and complement sys
- evasion of recognition by CD4 and CD8 cells
viral mechanism of injury
- prevent synthesis of macromolecules in host
- production of degradative enzymes and toxic proteins
- antiviral immune responses
- transformation of infected cells
tropism
- ability for virus to infect certain cells only
- match for receptors on the body human body and the virus
mechanisms of bacterial injury
- bacterial virulence
- bacterial adherence to host cells via adhesions and pili
- toxins
what factors impact bacterial virulence
- ability to adhere to host cells
- ability to invade cells/ tissues
- ability to deliver toxins
what are adhesins
- bacterial surface proteins
- allow bacteria to bind to host cells or ECM
pili
- proteins in surface of bacteria
- act as adhesins
what are bacterial endotoxins
- lipopolysaccharide in outer membrane
- stimulates host immune response and injuries of host
what type of bacteria produce endotoxins
gram-negative bacteria
what are exotoxins
- produced during normal growth and metabolism of bacteria
- secreted or released following lysis
what type of bacteria produce exotoxins
gram positive bacteria
examples of acute viral infections
- measles
- mumps
- poliovirus
- viral hemorrhagic fevers
examples of chronic productive viral infections
- HBV
- HIV
examples of chronic latent viral infections
- HSV
- VZV
- CMV
examples of transforming viral infections
- EBV
- produce cancers
measles
- affects multiple organs
- severity ranges from self limited to severe
- leading cause of vaccine preventable death and illness worldwide
how is measles transmitted?
respiratory droplets
pathogenesis of measles
- replication of virus in respiratory tract/ lymphatic tissue
- viremia and systemic dissemination
- T cell mediated
- antibody mediated immunity to protect against reinfection
what is responsible for the measles rash
T cell mediated response
what is another name for measles
rubeola
mumps
- acute systemic viral infection
- pain and swelling of salivary glands
- vaccine has reduced incidence greatly in US
what are clinical symptoms of mumps
- pain and swelling of salivary glands
- aseptic meningitis
- orchitis
- pancreatitis
what type of virus are the measles and mumps viruses
paramyxovirus family
pathogenesis of mumps
- upper respiratory tract infection
- lymph node infection and dissemination into blood stream
- salivary gland swelling and pain
how is polio transmitted
fecal oral route (enterovirus)
poliovirus pathogenesis
- ingested
- replicates in mucosa of pharynx and gut
- moves through lymphatics to lymph nodes then blood
- causes viremia and fever
- antibodies control disease in most cases
poliovirus symptoms
- mostly asymptomatic
- 1% of pts it invades CNS and replicates in motor neurons
- can cause spinal polioyelitis or bulbar poliomyelitis
spinal poliomyelitis
- paralysis of limb muscles
- especially affects kids
what disease does polio mimc
guillian barre syndrome
viral hemorrhagic fever pathogenesis
- life threatening multisystem syndrome -> vascular dysregulation and damage -> shock
- infect endothelial cells, macrophages and dendritic cells -> cytokine released
- reduced ability of dendritic cells to present antigen
- damage to BV -> hemorrhage
how are viral hemorrhagic fevers transmitted?
through infected insects or animals
what viruses cause viral hemorrhagic fevers
- enveloped RNA viruses
- arenavirus
- filovirus
- bunyavirus
- flavivirus
mild symptoms of viral hemorrhagic fevers
- fever
- HA
- rash
- myalgia
- neutropenia
- thrombocytopenia
severe sx of viral hemorrhagic fevers
- life threatening hemodynamic deterioration
- shock
what type of virus is the herpes virus
- dna virus
- establishes latent infection
classifications of HSV
- alpha herpesvirinae
- beta herpesvirinae
- gamma herpesvirinae
what are examples of alpha herpesvirinae
- HSV type 1
- HSV type 2
- varicella zoster
what are examples of beta herpesvirinae
- cytomegalovirus
- human herpes virus type 6
- hyman herpes virus type 7
what are examples of gamma herpesvirinae
epstein barr virus
HSV pathogenesis
- replicate in skin and mucosa membrane
- viral multiplication
- lysis of epithelial cells -> ulcers
where do HSV and varicella reside
- usually trigeminal nerve
where does cytomegalovirus usually reside
monocytes
where does EBV usually reside
b cells
HSV 1
- cold sores
- gingivostomatitis
- major cause of corneal blindness and fatal encephalitis
HSV 2
- genital sores
- can lead to life threatening disseminated visceral infections and encephalitis
how is varicella zoster virus transmitted
- respiratory aerosols
- gets into blood and causes skin lesions
acute infection of VZV
chickenpox
reactivation of VZV
- shingles
- innervated by trigeminal ganglia
- see blisters in specific dermatomes
other manifestations of VZV
- interstitial pneumonia
- encephalitis
- transverse myelitis
- necrotizing visceral lesions
cytomegalovirus
- infects monocytes and bone marrow progenitors
- in healthy typically asymptomatic
- in neonates and immunocompromised can cause serious systemic infection
- most common opportunistic viral pathogen in AIDS
how is cytomegalovirus transmitted
- saliva
- sexually
- transplacentally from pregnant mother to unborn baby
- blood transfusions or organ transplants
- during childbirth
typical symptoms of CMV in infants
- deafness and mental retardation
typical symptoms of CMV in immunosuppressed
- pneumonitis
- hepatitis
- choriorentitis
- meningoencephalitis
cytomegalic inclusinon disease
- caused by CMV
- IUGR
- hemolytic anemia
- jaundice
- encephalitis
oncogene viruses
- EBV
- HPV
- HBV
- HTLV-1
EBV infection outcomes
- infectious
- lymphadenopathy and splenomegaly
- lymphomas
- infect B cells -> proliferate -> thrombocytopenia
- nasopharyngeal carcinomas
- resolves in most pts with in 4-6 weeks
lymphomas associated with EBV
- burkitt
- hodgkin
s. aureus infections
- skin lesions
- abscesses
- sepsis
- osteomyelitis
- pneumonia
- endocarditis
- food poisoning
- toxic shock syndrome
what type of bacteria is staphylococcus
gram positive cocci
why can staphylococcus result in toxic shock syndrome
- contains superantigens
- superantigens cause inappropriate and excessive stimulation of T cells
ways staphylococcus evades infection
- surface receptors binding to endothelial cells
- superantigens
- surface A protein
- bacterial toxins
- capsule and biofilm
types of streptococcus
- alpha hemolytic
- beta hemolytic
types of alpha hemolytic streptococcus
- s. pneumoniae
- viridans streptococci
types of beta hemolytic streptococcus
- s. pyogenes
- s. agalactiae
s. pneumoniae
- alpha hemolytic streptococcus
- common cause of community acquired pneumonia in elderly
- causes meningitis in kids and adults
viridans streptococci
- alpha hemolytic streptococcus
- found in normal oral flora
- common cause of endocarditis
s. pyogenes
- beta hemolytic streptococcus
- pharyngitis
- scarlet fever
- erysipelas
- impetigo
- rheumatic fever
- toxic shock syndrome
- glomerulonephritis
s. agalactiae
- beta hemolytic streptococcus
- colonizes in female genital tract
- causes spesis and meningitis in neonates
- chorioamnionitis in pregnancy
ways that steptococcus evades immune response
- m protein
- protein F
- streptokinase
- pneumolysin
- hyaluronic acid capsule
m protein
- prevents phagocytosis
- binds fibrinogen and complement proteins
protein F
- mediates adhesion to fibronectin
- fibronectin is ECM protein
streptokinase
- cleaves plasminogen to activate plasmin
- dissolves clot
pneumolysin
inserts into host cell membrane and lyses cell
diptheria
- caused by corynebacterium diptheriae
- transmitted by respiratory droplets or skin exudate
ways that diptheria evades immune response
- AB toxin which blocks protein synthesis
- forms pseudomembrane
pseudomembrane in diptheria
- exotoxin
- causes necrosis of epithelial cells
- liberates serous and fibrinous material
types on neisserial infections
- n. meningitidis
- n. gonorrhoeae
n. meningitidis
- causes meningitis in adolescents and young adults
- transmitted through respiratory route
- most can eliminate infection
- antigenic variation
how does n. meningitidis evade immune response
- covered in capsule
- capsule inhibits opsonization and destruction by complement system
n. gonorrhoeae
- 2nd most common STD
- infection in urogenital tract by interacting with epithelial cells -> cellular invasion
- causes PMN
- arthritis, meningitis, and neonatal opthalmia
who is more likely to become infected by nisseria
- people who lack complement proteins that form MAC
pertussis
- gram negative coccobacillus
- highly communicable
- produces AB toxin
- inhibit neutrophils and macrophages
- paralyzes cilia
what is another name for pertussis
whooping cough
what are possible outcomes of severe bordetella infection
- laryngotracheobronchitis causing:
- bronchial mucosal erosion
- hyperemia
- copious mucopurulent exudate
- lymphadenopathy
p. aeruginosa
- gram negative bacillus
- deadly in people with CF, severe burns, neutropenia
- very resistant to antibiotics
- common hospital acquired infection
possible clinical outcomes of p. aeruginosa
- corneal keratitis in contact lens wearers
- endocarditis and osteomyelitis in IV drug users
- external otitis
how does p. aeruginosa evade immune response
- excrete exotoxin A -> inhibits protein synthesis
- elastase
- leukocidin
- hemolysins- destroys cell membranes
what is the evidence of infection in Tb
- fibrocalcific pulmonary nodule at site of infection
- can lay dormant for years
what affects outcome of Tb
- T cell mediated immunity
- causes pathologic lesions like caeseating granulomas and cavitation
where does Tb infection reside/ replicate
macrophages
what is the ghon complex
- parenchymal lung lesion
- nodal involvement
pathogenesis of Tb
- 3 weeks post infection IL12 released by dendritic cells
- Th1 response
- release IFN gamma
- macrophages activated
- granuloma and caseous necrosis
primary Tb
develops in previously unexposed person
secondary Tb
- develops in previously sensitized host
- usually involves apex of upper lobes of one or both lungs with cavitation
systemic symptoms of Tb
- related to cytokine released by activated macrophages
- malaise
- anorexia
- weight loss
- low grade fever
- night sweats
late stages of Tb
- increasing amounts of sputum, hemoptysis, pleuritic pain
dx of Tb
- history
- xrays
- gold standard= sputum culture
syphilis
- chronic STD
- varied clinical sx
- caused by spirochete tryponema pallidium
primary syphilis
- 3 weeks after contact
- chancre on penis, cervix, vaginal walls, or anus
- heals without therapy
secondary syphilis
- 2-10 weeks post exposure
- widespread mucocutaneous lesions in oral cavity, palms of hands, soles of feet
- lymphadenopathy
- mild fever
- malaise
- weight loss
tertiary syphilis
- long latent period (5 years)
- CV syphilis
- neurosyphilis
- benign tertiary syphilis
CV syphilis
- aortitis
- aortic valve insufficiency
neurosyphilis
- meningovascular disease
- diffuse brain parenchymal disease
- CSF abnormalities
- increased protein
- decreased glucose
benign tertiary syphilis
- gummas in bone, skin, and mucous memrbanes
- gummas are bumps/ elevations
what causes lyme disease
- borrelia burgdorferi
- can be persistent or severe
how does lyme disease evade immune response
antigenic variation
what causes damage from lyme disease
- host immune response
- does NOT produce toxin
- T cell and cytokine release mediates immune response
- antibodies made 2-4 weeks post infection
- direct complement mediated phagocytosis and killing of bacteria
