Unit 6: Flashcards
(125 cards)
1
Q
what are the major groups of infectious organisms
A
prions, viruses, bacteria, fungi, parasites
2
Q
what is a parasite
A
organisms which live within another living organism at whose expense it obtains some advantage
3
Q
what kinds of organisms are most often parasites
A
protozoa, metazoa, arthropods
4
Q
least to most complex infectious agents
A
prions, viruses, intracellular bacteria, mycoplasma, bacteria, fungi, protozoa, metazoa + arthropods
5
Q
what are obligate intracellular organisms
A
- require a host cell to grow and multiply using its metabolic machinery
- tend to infect parenchymal cells
- include viruses, prions, rickettsiae and chlamydiae
6
Q
extracellular organisms
A
- multiply outside of a host cell
7
Q
facultative intracellular organisms
A
- can grow inside and outside of cells
- include mycobacteria and some fungi
8
Q
what is morbidity
A
the degree to which a disease can impair normal functioning
9
Q
what is mortality
A
the state of being subject to death
10
Q
what’s case fatality
A
specific measure that calculates the proportion of deaths from a disease against the total number of diagnosed cases
11
Q
what is an epidemic
A
the occurrence of cases of a disease exceeds what was normally expected
12
Q
what is infectivity
A
the ability of an organism to colonize tissues
13
Q
what is pathogenicity
A
the ability of an organism to cause disease
14
Q
low vs high grade pathogens
A
low grade = only cause disease in immunocompromised hosts (opportunistic infections)
high grade = virulent pathogens, cause disease in even healthy hosts
15
Q
how does an organism gain entry into the body
A
through natural passages
- typically mucosal or epithelial barriers
- portals of entry = skin, respiratory tract, urogenital tract
- can also gain entry via trauma and direct inoculation
- heart, bones, brain and muscle can only be infected via the blood
16
Q
4 principle methods of spread of infection…
A
- physical contact
- airborne infection
- food-borne infection
- insect-borne infection
17
Q
when a microorganism enters a tissue 3 things can happen…
A
- the invader dies due to non-specific and specific defences (most common)
- the invader may survive without giving rise to obvious clinical disease, but cause an immune response
- the invader survives, multiplies and produced clinical disease
18
Q
the pathogen itself plus the host and environment influence the outcome of exposure to a pathogen…
A
the pathogen: the virulence and dose of its exposure
the host/environment: the status of the primary defences of the host and the immune status of the host
19
Q
when does infection occur
A
when an infectious agent has entered and multiplied in a host
- infect does not necessarily mean disease
20
Q
subclinical infection
A
development of an immune response but disease is not clinically apparent
21
Q
clinically apparent infection
A
when the infectious agent has survived and multiplied in the host, causing tissue damage
22
Q
example of infection spread more widely: poliomyelitis
A
- the casual enterovirus enters via the intestinal tract but there is no sign of intestinal infection
23
Q
how can you diagnose different infections in the bloodstream
A
- viremia, bacteremia and fungemia can be diagnosed using blood cultures, serology and molecular techniques
- parasitemia is diagnosed by identifying the parasite in blood smears
24
Q
what is bacteremia
A
- the presence of viable bacteria in the bloodstream
2 types… - transient bacteremia = body removes small numbers of bacteria in the bloodstream
- severe bacteremia = large numbers of bacteria in the bloodstream are capable of overwhelming the body’s defences
25
what is toxemia
presence of toxins produced by bacteria within the bloodstream
26
what is sepsis/septicemia
a disease state that arises from the presence of bacteria or their toxic byproducts in the blood
- results in a clinical syndrome characterized by fever, vasodilation and decreased BP
- in these cases, subsequent shock and DIC result in death
27
what are virions
free inactive virus particles
28
general structure of viruses
- central core of nucleic acids
- protein coat or capsid
- an outer lipid envelope in some
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virus life cycle and how they invade cells
- virus binds to receptors on cell via viral surface ligands
- virus penetrates cell by fusion, endocytosis or translocation
- virus is uncoated inside the cell and genome separates
- virus initiates translation and transcription
- new viral protein s are made
- new virions are assembled and released directly or by budding
30
tropism of poliomyelitis and HepA
poliomyelitis = motor neurone of the CNS
Hep A = cells of the liver
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how do viruses cause injury to their host
viral mediated cell necrosis, via either...
1. viral mediated cytopathic injury
2. Virally mediated alteration of apoptosis pathway
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examples of viral mediated cytopathic injury
- cell lysis: occurs during virus replication and release, interferes with cell function
- inhibition of DNA, RNA or protein synthesis: causes subtle cell dysfunction or death
- direct insertion of viral proteins into membrane: alters membrane function/integrity or promotes fusion with neighbouring cells
33
what are inclusion bodies
assembled viral particles formed during viral replication
- can occur in cytoplasm or nucleus
- in rabies virus infection produces eosinophilic inclusion bodies in the cytoplasm of neurons
34
what are cytopathic viruses
viruses that cause extensive necrosis or target cells and result in cell death
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cytopathic virus example: Ebola virus
- a filovirus which causes necrosis resulting in disseminated hemorrhage (and shock) and DIC
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what are filoviruses
enveloped RNA viruses that are highly cytopathic and result in cytolysis
- spread between humans is by contact with secretions or reuse of undterblized needles
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what are persistent/chronic viral infections
viruses that result in slow and progressive cell death
- examples are HepB and HepC
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what is Cirrhosis
loss of normal lobular architecture of the liver as a result of necrosis, scarring by fibrosis and nodular regeneration
- may occur with chronic intoxication, leads to diminished liver function
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examples of virally-mediated alteration of apoptosis pathways
- host cells mat undergo self-directed apoptosis to control and eliminate infected cells
- some viruses encode genes that impair apoptosis to promote persistent viral infection
40
the antiviral immune response
- obligate intracellular pathogens induce an acute response with lymphocytes, plasma cells and macrophages
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how does the body attempt to eliminate a virus
- viral proteins on the surface of the host are recognized as foreign by cytotoxic T cells
- this induced a cell-mediated immune response and cytolysis
- the body attempts to eliminated virally infected cells - the host response may result in cell death and associated illness
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hepatocellular loss associated with HepB is mediates by...
cytotoxic T-cell mediated cytolysis
43
how the body produces IFN as a response to viral infection
- IFN is produced by helper T cells in the Th1 response
- the antiviral effects of IFN are due to interference of viral translocation
- IFN is also secreted by fibroblasts and macrophages following exposure to a virus
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the presence of what suggests response to a viral pathogen rather than a bacterial pathogen
lack of neutrophil response and increased number of lymphocytes that accompany viral infection
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virally induced transformation
transformation causes cells to become immortal and grow independently of growth-regulating signals
- results in cancer
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what is the EBV
a herpes virus which causes several neoplasms such as nasopharyngeal carcinoma and Burkitt's lymphoma
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what are latent viral infections
- when viral genes remain in surviving target cells for long periods but are not expressed
- lead to disease later in life
- commonly associated with neoplastic transformation
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properties of herpes virus
- causes latent infections, most prevalent virus in the population
- large double stranded DNA viruses
- ubiquity of herpes infection is related to their inability to remain latent and that they are highly contagious
- HSV-1 causes oral lesions, HSV-2 causes genital lesions
49
how does chickenpox in childhood lead to shingles in later life
- the casual herpes virus may remain dormant for years in neurone and then be reactivated causing shingles
- shingles is caused by reactivated virus travelling down sensory nerves
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outcomes of viral infection
- acute cytolysis or necrosis of target cells may result in organ dysfunction or death
- outcome of less severe infection is most likely survival
- recovery is associated with an appropriate immune response that neutralizes the virus
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complication of viral infection: secondary bacterial infection
- cell death or dysfunction provides "fertile soil" for other pathogens to root
- viruses that injure epithelium of upper airways can cause paralysis or loss of surface cilia which impairs cellular machinery, can lead to secondary infection
52
what do rickettsiae and chlamydiae have in common
- both are obligate intracellular bacteria
- cellular response to these organisms is mononuclear
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what is trachoma
the leading cause of blindness - a severe conjunctivitis leads to eventual scarring and opacification of the cornea
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what causes non-gonococcal urethritis
chlamydia trachomais
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how does chlamydia cervicitis affect infants
leads to neonatal ophthalmia when an infant passes through the birth canal, causes purulent inflammation of the conjunctiva of the eyes of newborns
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Psittacosis
- casual agent is Chlamydophilia psittaci
- disease passed from bird to man
- birds are the reservoir of infection
- transmission to man is by infected droplets
- in man symptoms are fever and interstitial pneumonia
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zoonotic diseases
diseases transmitted from animal to man
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The rickettsiae mode of infection
- require arthropod vectors for transmission - includes ticks, lice and mites
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what is typhus
- a rickettsiae infection
- R. prowazeckii are the casual agent
- reservoir of infection = rats
- organism injures the vascular endothelium, leading to thrombosis and hemorrhage
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examples of rickettsial diseases
- typhus
- rocky mountain spotted fever
- Q fever
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infection by facultative intracellular organisms
- include mycobacteria and fungi
- many mycobacteria remain asymptomatic and dormant in macrophages
- immune suppression leads to reactivation of these infections
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how do prions differ from viruses
they lack RNA and DNA
- considered sub viral transmissible agents - consist of protein only
63
what are the casual agents of spongiform encephalopathies
prions
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what does spongiform refer to
vacuolar degeneration in the brain
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how do prion associated diseases develop
- when normal prion proteins change to abnormal prion protein
- accumulation of this abnormal protein leads to dysfunction of the affected brain tissues and neuronal loss
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what is unique about prions diseases
- there is no inflammatory response to prions
- all diseases are slow, degenerative neurologic diseases
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Bovine spongiform encephalopathy transmission
a chronic wasting disease that can be transmitted from cattle to man by consumption of infected beef
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what is the commensal flora
- bacteria that are normally resident in the body (the microbiome)
- compete with growth factors to combat virulent organisms
- in ruminant stomachs allows normal digestion of cellulose
69
what is dysbiosis
- changed composition of the microbiome due to disease, antibiotics or diet changes
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what are opprotunistic bacteria
the normal flora that has become pathogenic if the host is immunosuppressed or if they gain access to part of the body where they don't belong
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what are bacteriostatic agents
antibacterial agents that inhibit growth or multiplication of bacteria
72
what are bactericidal agents
antibacterial agents that kill bacteria
73
why must antibiotics be taken for their whole course
if stopped early the surviving organisms may lead to growth of larger numbers
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what 2 things must you ensure before using antibiotics
1. the disease to treat is of bacterial origin
2. the sensitivity of the organism to specific antibiotics is determined
75
what is the role of antibiotics
to inhibit growth of or kill BACTERIA
76
antibiotic-resistant strains of bacteria
mutate/adapt to change induced by the antibiotic
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what are the 3 things bacterial virulence depends on
1. adhering and colonizing host cells
2. invading the cell to release locally and remotely acting toxins
3. the production go local vasculitis
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how do gram positive cocci cause tissue injury
they have fibrillar surface M proteins to prevent their phagocytosis by macrophages
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how do facultative intracellular bacteria cause tissue injury
- have restricted tropism to infect epithelial cells and/or macrophages
- they bind to membrane integrins or ECM proteins such s fibronectin or collagen
80
what are the 3 main bacterial virulence factors
1. bacterial adhesins: cell-surface components that facilitate adhesion to cells in the host they infect
2. bacterial toxins: endotoxins (on the bacteria) and exotoxins (secreted by the bacteria)
3. bacterial enterotoxins:exotoxins that exert their effect on intestinal mucosal cells
81
what are the bacterial defences that increase their virulence
plasmids, bacteriophages, biofilms, quorum sequencing
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bacterial Adhesins characteristics and mode of action: mycoplasma example
- mycoplasmas are extracellular bacteria that lack a cell wall
- species of this bacteria can cause pneumonia, infertility and abortion
- Mycoplasma hemofelis changes parasitic in cats - bacteria multiply and changes in RBCs cause phagocytosis to destroy the RBC (hence the bacteria)
- causes severe anemia and eventually death
83
why os mycoplasma difficult for the immune system to detect
- it can remain dormant in macrophages in the spleen until the cat is immunosuppressed with feline ID virus
84
Lipopolysaccharide as an endotoxin
- LPS is part of the cell wall of gram-negative bacteria
- they are released into the blood of the host following death and lysis of bacteria
- response to LPS is cytokine and chemokine release to activate T cells
- TNF is a cytokine that exerts effects on small blood vessels
85
what are the effects of TNF on small blood vessels as a to response to LPS
- generalized peripheral vasodilation - progressing to shock
- endothelial injury and activation of coagulation cascade - leads to DIC and ARDS
- systemic acute phase response and fever
- local vasculitis - results in thrombosis of small blood vessels
86
what can endotoxic shock accompany
- severe urinary tract infection
- intestinal surgery
- gram-negative bacteria infection
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locally acting vs remotely-acting exotoxins
locally acting
- enzymes that are secreted into their immediate environments
- breakdown material for bacterial metabolism
- useful for tissue invasion - cause local tissue injury
remotely acting
- enzymes absorbed into the bloodstream and mediate their effects at distant sites
- induce formation of antitoxins
- heat-liable - destroy by cooking
88
locally acting exotoxins example 1: Staphylococcus Aureus
- exotoxin it produces = coagulase
- coagulase converts fibrinogen into fibrin
- coagulase causes bacterium to be coated with fibrin and resist phagocytosis
- causes pus o form in tissues
- cause of secondary bacterial pneumonia, following primary viral respiratory illness
89
locally acting exotoxins example 2: Clostridium perfringens
- gram positive anaerobe in soil and intestinal tract
- after death it is released from the intestinal tract, invades tissues of cadavers
- can be isolated from cases of gas gangrene
- produces gas and acid by breaking down sugar in muscles
- produces wide variety or enzymes that act locally - exotoxins = hyaluronidase, collagenase, hemolysins and lecithinase
- net effect of these enzymes = production of inflammation with gas production
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examples of bacteria that produce exotoxins
Staphylococcus aureus - toxic shock syndrome
Streptococcus pyrogens - erythrogenic toxin
Group A streptococci - necrotizing fasciitis
Corynebacterium diphtheriae - diphtheria toxin
Clostridium tetani - tetanus toxin
clostridium botulinum - botulism toxin
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remotely acting exotoxin example 1: toxic shock syndrome by Staphylococcus aureus
- proliferation of this bacteria in the vagina is associated with the use of high absorbent tampons
- TSST is a bacterial super-antigen: causes cytokine release, fever, capillary leakiness, shock and multi-system organ failure
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remotely acting exotoxin example 2: necrotizing fasciitis by group A streptococci
- bacteria secrete an exotoxin which causes a rapid necrosis process and spreads to subcutaneous tissue - may extend to deep fascia
- Thrombosis of vessels and secondary cutaneous gangrene also occur
- systemic signs include leukocytosis, fever, chills and exhaustion
- skin and underlying tissue becomes discoloured, gangrenous and septicemia develops
- if necrosis is extensive, antibiotics cannot penetrate and surgical resection of tissue is needed
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what are bacterial enterotoxins
- exotoxins that exert their effect on intestinal mucosal cells
- produced by bacteria during multiplication within the gut or within food
- attach to gut mucosal receptors and cause damage/altered function
- cause diarrhea, cramping and abdominal pain
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enterotoxin example 1: Cholera
- disease caused by vibrio cholerae which secretes an enterotoxin
- enterotoxin leads to isometric fluid secretion by intestinal cells because of increased cAMP
- diarrhea leads to loss of water and electrolytes - death can result from dehydration, electrolyte imbalance or shock
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enterotoxin example 2: Hamburger disease
- disease caused by E. coli O157:H7 - acquired through improperly cooked ground beef
- causes abdominal pain, diarrhea and bloody diarrhea - lead to hemolytic ureic syndrome
- E. coli O157:H7 secretes a verocytotoxin which effects vascular endothelial cells - leads to thrombosis in the GI tract and kidneys
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enterotoxin example 3: food poisoning
- refers to acute gastroenteritis caused by bacterial toxins in contaminated food or drink
- causes vomiting and severe diarrhea
- bacteria in the food multiply and produce toxins in the bowel = signs 12-24 hours later
- bacteria in food produce toxins which are ingested = signs appear 2-6 hours later
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what is the bodies repose to bacterial infections
suppurative inflammation
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what is suppurative inflammation
- acute inflammation that follows bacterial infection
- characterized by liquefactive necrosis and the formation of pus
- increases vascular permeability allowing an increased number of neutrophils
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what is appendicitis
the result of obstruction of the lumen of the appendix, increased intraluminal pressure results in ischemic injury
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hardware disease of cattle
- pieces of hardware get trapped in the all of the reticulum and it is punctured
- metal travels to the pericardial sac and carries bacteria along its path there
- once in the pericardial sac, severe fibrinopululent inflammation can lead to the accumulation of fluid in the heart
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what is suggestive of bacterial infection
- purulent inflammation
- suppurative inflammation
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what are Koch's postulates
1. the organism is found in all disease lesions
2. the organism can be grown and isolated in culture
3. secondary inoculation of the purified organism from culture causes the same lesions in experimental animals
4. the organism can be recovered from the experimental animal
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systemic vs superficial fungal diseases
Systemic = rare
- affect the "deeper" tissues
Superficial = common
- include athletes foot, ring worm and vaginal yeast infections
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organisms that cause systemic fungal disease
histoplasmosis, coccidiodomycosis, blastomycosis
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what kind of infections are fungal nfectiosn
opprotunistic infections
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why do antibiotics increase incidents of fungal infections
- antibiotics disrupt the normal flora which is needed to limit fungal growth
- immunosuppressive therapy also favours opprotunistic fungal infections by suppressing cell-mediated immunity
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how do fungi cause tissue injury
- they induce the DTH hypersensitivity response to fungal antigens
- DTH produces granulomatous lesions
- some fungi can directly invade small blood vessels leading to thrombosis and necrosis of adjacent tissues
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what is dermatomycoses
- patchy, red, scaly lesions affecting the skin between fingers and toes or in groin area
- highly contagious and difficult to treat
- ring-like lesions on the scalp cause patchy hair loss
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Fungal pathogen example: Candida albicans
- the fungus that most often causes disease
- commensal organism on the mucous membrane - found at oral cavity and GI tract
candida can overgrow = opprotunistic bacterium
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different hosts of parasites
definitive host = host of the mature parasite
intermediate host = host of the immature parasite
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major types of parasites
protozoa, helminths and ectoparasites (arthropods)
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what helps control parasitic infections
the role of type I (IgE mediated) and type IV (cell mediated) hypersensitivity reactions
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protozoal parasites
- dominate as causes of infectious disease
- difficult to treat infections because of the variety of forms they assume in their host
- transition either via insect vectors or ingestion
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toxoplasmosis: protozoal parasite
- definitive host = cats
- cats excrete oocysts in their feces which mature and become infectious
- intermediate hosts = humans and animals
- disease follows when they ingest infectious oocytes
- cause fever and lymphadenopathy that can be followed by cerebral dysfunction
115
effects of toxoplamosis
- cerebral toxoplasmosis: characterized by the presence of organisms in the brain along with mononuclear cells and necrosis
- oocytes can encyst in the SI and infect villus enterocytes
- can cause fetal infection transplacentally - organism affects fetal brain and retina leading to necrosis and scarring
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what are helminths
- multicellular parasites
- include the nematodes, cestodes and trematodes
- usually NOT opprotunistic pathogens
. man can act as a natural or accidental host
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type of helminths: nematodes (round worm)
- don't require an intermediate host
- cause pinworm disease, trichinosis and filariasis
- pinworms cause anal irritation in children
- trichinosis causes acute myositis and inflammation of muscles
- filariasis requires culex mosquito for transmission
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what his elephantiasis
obstruction and enlargement of tissues due to adult worms present int he lymphatics
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helminth parasite: hookworm disease - ankylostomiasis
- acquired when larvae burrow through the skin of feet and enter veins
- carried int eh blood to the lungs when're they reveal to the pharyngeal area and are swallowed
- finally reach the small intestine and attach to mucosa to feed by sucking blood
- blood loss leads to iron deficiency and anemia
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helminth parasite: roundworm disease - ascariasis
- acquired when eggs of the parasite are ingested
- when eggs reach the intestine, larva penetrate the intestinal wall and mature
- obstructs the bowel and causes inflammation of bile and pancreas ducts
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type of helminths: cestodes (tapeworm)
- spend part of their life cycle in man and part in another animal
- in cystic stage in animal host
- man is infected by improperly cooked meat
- once in man, worm matures and reproduces sexually in the small inestine
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dog tapeworm
- passes its adult stage in the intestine of dogs
- man is infected by consuming dog contaminated vegetables
- dogs are infected when they consume infected sheep of other livestock
- in man, cystic stage causes hydatid disease - forms large cysts (fatal)
123
type of helminths: trematodes (flukes)
- flat worms require an intermediate host (often snails)
- adult flukes live in the veins of pelvis and bladder
- eggs are laid in the wall of the bladder and produce intestine inflammatory reaction - leads to blood in urine
- most common disease caused by flukes = schistosomiasis
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what are ectoparasites
- live on the skin and cause itching
- scratching leads to injury of the skin
- examples are scabies, lice and fleas
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Arthropods as external parasites
- important disease carriers
- individuals develop hypersensitivity reactions to their bites
- can act in 2 ways
1. Mechanical vector: pick up infecting agents and deposit them
2. Biological vector: helps complete the life cycle of the infecting agent - e.g. flea allergy dermatitis in animals
