Pathogens and the Host Flashcards by Helena Gibbons-Wood

What are signs and symptoms of clinical infection?

inflammation
pain
pyrexia
tachycardia
rigors
increased white cell count
Increased C reactive protein (CRP)

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What is a pathogen?

organism that can cause disease

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What is a commensal?

A commensal is an organism which is part of normal flora e.g. E. coli in the gut, Staph aureus in the nose, axilla

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How do we know if organism is a pathogen or commensal?

koch’s postulates:
organism must be found in all cases of the disease
able to be cultured outside the body for several generations
should reproduce the disease on inoculation

sterile vs non-sterile sites

knowledge of
normal flora for site
organism’s pathogenicity
clinical context

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What is pathogenicity?

The capacity of a micro-organism to cause an infection

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What are requirements for pathogenicity?

infectivity- ability to become established

virulence- ability to cause harmful effects once established

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How is infectivity achieved?

Attachment
E. coli-
P-fimbriae
Receptor on uroepithelial cells

Acid resistance
Helicobacter pylori-
Urease
Makes ammonia from urea

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How is virulence achieved?

Conferred by virulence factors
Genetically determined microbialcomponents-
Invasiveness
Toxin production
Evasion of immune system

specific to strains not species (staphaureus does not share same pathogenicity as other staphylococci)

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How is invasiveness achieved in streptococcus pyogenes (Group A streptococci)?

connective tissue breakdown
-hyaluronidase
-collagenase

fibrinolysis
-streptokinase enzyme

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Describe exotoxins?

released extracellularly by the micro-organism

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Describe endotoxins?

structurally part of the gram negative cell wall

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Describe enterotoxins?

exotoxins which act on the GI tract

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Describe the exotoxin: Tetanus?

Clostridium tetani (obligate anaerobe)

Infection of dirty wounds

Toxin production:
Binds to nerve synapses
Inhibits release of inhibitory neurotransmitters

Death caused by respiratory paralysis

Treated by debridement, antibiotics and antitoxin

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Describe the enterotoxin: Cholera?

Vibrio cholerae-
Colonises small intestine

Enterotoxin production:
Increases cAMP levels
Inhibits uptake of Na+ and Cl- ions
Stimulates secretion of Cl- and HCO3- ions
Passive (massive) outflow of H2O

Causes death by dehydration

Treated by rehydration

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Describe super antigens?

Certain exotoxins of Strep pyogenes and Staph aureus
Able to stimulate division of T cells in the absence of specific antigen
Overwhelming cytokine production causes “toxic shock”

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How is endotoxin structured?

Component of the Gram-negative bacterial cell wall:

Lipopolysaccharide-
Lipid A -THE NASTY PART
Oligosaccharide core
Specific polysaccharide chain

What is meaning of MRSA and MSSA staphylococcus aureus?

MRSA- methicillin resistant staph aureus
MSSA- methicillin sensitive staph aureus

Why is staphylococcus aureus commonly penicillin resistant?

due to beta lactamase

Describe clostridium perfringens? (gram positive bacilli)

Found in soil and normal commensal in human and animal gut/faeces

in contaminated food, can cause food poisoning (enterotoxin-producing strains)

in serious wounds (wartime) can cause “gas gangrene”

What are three characteristic ways by which virus causes pathogenesis in the host?

Cell destruction following virus infection
-Death of T4+ cells by HIV

Virus-induced changes to cellular gene expression
-Cellular transformation by tumour viruses

Immunopathogenic disease
-Influenza A virus.
-Coxsackievirus-induced myocarditis

How does virus enter cell?

respiratory tract
alimentary tract
urinogenital tract
arthropod vector
capillary
skin
conjunctiva

Describe an acute infection?

so after person gets infected, there is a peak up and down. Virus production is high and the human response dominates and is able to control infection.

Describe latent infection?

after acute infection, the virus goes and hides away and keeps dormant for ages. After certain stimulus it comes back and attacks exactly the same as original acute infection attack

Describe chronic infection?

after acute infection, the virus load doesn’t go back to basic level (doesn’t disappear) and virus remains above baseline for life.

Describe tumour virus infection?

acute infection is mild or very little and virus remains in very low level in background causing very slow changes in cell until becomes malignant .

Give examples of acute virus infections?

Influenza A virus- respiratory infection enterovirus- enteric and neurological infections

What is viraemia?

means virus reaches the blood stream

How does pathogenicity occur in Influenza A?

Virus infects cells of the respiratory tract Destruction of respiratory epithelium -Secondary bacterial infections Altered cytokine expression leading to fever -e.g interleukin-1 and interferon -Avian influenza virus (H5N1) causes a “cytokine storm”

Describe antigenic drift?

Minor changes (natural mutations) in the genes of flu viruses, occurs gradually over time to generate antigenic variants

Describe antigenic shift?

Abrupt major changes in virus antigenic structure

How is the generation of novel influenza brought about?

non human hosts for influenza A viruses play a key role in generating new virus types e.g. avian influenza, swine influenza

Give examples of enterovirus infections?

Poliomyelitis (poliovirus) Aseptic meningitis (many enteroviruses) Myocarditis (coxsackie B viruses) Pancreatitis (coxsackie B viruses) Respiratory infections (many enteroviruses)

Mechanisms of enterovirus?

acquired through GI system, goes to gut and from the gut, it goes into the bloodstream by viraemia. Either goes to non neuronal tissue (heart...pancreas) or neuronal tissues (CNS) (that can cause paralysis). Virus in gut gets excreted in stools

Give example of latent virus infection?

herpes simplex virus- cold sores (type 1 ) and genital lesions (type 2)

Describe the herpes virus infection?

virus infects the epithelium and cold sore happens after this episode, virus migrates to nerve ganglia and virus latent in nucleus then a stimulus occurs and virus gets reactivated and migrates to epithelium. Leads to virus replication

Give examples of virus-induced tumours?

Papillomaviruses (HPV)-cervical carcinoma Retroviruses- lymphomas and leukemias

Describe the retrovirus replication cycle?

Virus attaches to cell by membrane fusion and uncoating process happens. Membrane fusion releases the viral nucleic acid material on its own in the infected cell. By a process of reverse transcription- RNA/DNA hybrid forms and then there is the viral DNA formed- double stranded DNA. This migrates into nucleus and integrates into host nucleic acid material and through viral DNA integration, provirus is formed.

Describe Human T-lymphotropic virus-1 (HTLV-1) (virus induced tumours)?

Transmission by blood and mother to child. Infects T cells Modifies host cell gene expression using a Transactivating protein (tax) Variety of diseases including leukaemia (Adult T-cell Lymphoma-Leukaemia) Directly responsible for the tumour.