General pathology of bacterial infections
GENERAL PATHOLOGY OF BACTERIAL INFECTION
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Bacteria may be extracellular or intracellular (Mycobacterium, Brucella)
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Contain both RNA and DNA
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Lack nucleus
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Lack few cytoplasmic organelles
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Reproduce by binary fission
Classification of bacteria
Based on morphological, cultural, biochemical, antigenic and nucleic acid parameters
Morphological appearance
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Round (micrococci) ; Chains of cocci (streptococci); Rods (bacilli); Filamentous with branching (Actinomyces)
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Some bacteria have cilia and flagella
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Staining characteristics– Based on Gram's staining classified as Gram’s positive & Gram’s negative
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Virulence or pathogenecity – Staphylococci & Streptococci live in the nasopharynx & skin of normal animals and cause disease through wounds or immunosuppressed animals; Other streptococci are not normal inhabitants and produce disease
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Some bacteria are highly invasive multiply and spread rapidly producing bacteraemia and septicaemia like Bacillus anthracis
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Localised infection develops either at the portal of entry or at different sites after systemic spread. Example - Clostridium tetani – at site of entry; Mycobacterium sp – spreads throughout the body and later becomes localized
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Ingestion of toxins found outside the body example Botulism and Staphylococcal food poisoning
Mechanism of bacteria causing disease
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Exotoxins
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Endotoxins
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Other bacterial products
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1.
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Complex lipopolysaccharides (LPS)
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Components of cell wall of Gram-ve bacteria
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Released on disintegration
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LPS is a long chain toxic fatty acid (lipid A)connected to a core sugar chain
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A carbohydrate chain is attached core sugar called O antigen which is used to serotype and differentiate bacteria
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2.
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3.
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LPS causes severe systemic effects
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4.
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5.
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6.
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Example of specific neurotoxins are :
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Tetanospasmin (Clostridium tetani)- blocks inhibitary transmitter substance
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Botulinum (Cl. botulinum)-blocks cholinergic neurotransmitters
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Alpha toxin (Cl. perfringens) -causes hemolysis and damages cell membrane -helps in spread of bacteria
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Lethal toxin (Anthrax)-stimulates macrophages to produce free radicals and cytokines like interleukin and tumour necrosis factor which induce systemic shock and death
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Exotoxins of anthrax bacilli and Escherichia coli causes ribosomal dysfunction leading to increase in cyclic AMP
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In low doses LPS activates macrophages which eliminate bacteria
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Activate complement- removal of bacteria
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LPS also enhances release of TNF and interleukins in large amounts which sets up a local inflammatory response and eliminate infection
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At higher levels of LPS, cytokine induces release of nitric oxide, platelet activating factor
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Systemic effects like fever occurs
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At still higher levels - septic shock or endotoxic shock due to systemic vasodilation, reduced cardiac output and activation of coagulation system resulting in Disseminated intravascular coagulation (DIC)
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Attachment and entry of bacteria
- Attachment of bacteria to the cell surfaces requires bacterial adhesins and cell receptors. Examples of bacterial adhesins are
- Fimbrial proteins (Escherichia coli, Salmonella sp.)
- Lipoteichoic acid (streptococci)
- M protein and lipoteichoic acid (Fimbriae of streptoccoci)
Bacteria tropism
- Fimbriae or pili in Gram negative bacteria are non flagellar filamentous structures
- At the tips of the pili are minor protein components that determine to which host cells the bacteria will attach Example: Escherichia coli
- Type L protein bind mannose (host receptor) causes urinary infection
- Type P proteins bind galactose and causes pyelonephritis
- Type S proteins bind sialic acid and causes meningitis
- A single bacterium can express more than one pili or many pilar adhesins
Host receptor substances
- Fibrinonectin (streptococci)
- Mannose (/strong> Escherichia coli )
Colonisation resistance
- It is an important defence mechanism wherein attachment of bacterial adhesins is inhibited by normal microflora which occupy or block receptor sites by producing toxic metabolites and bacteriocins
Penetration
- Some bacteria, reach the target cells and do not penetrate further (E.coli,Vibrio cholerae)
- Others cross surface membranes after endocytosis by epithelial cells or go between cells (Salmonella, Brucella)
- Inhaled facultative bacteria are taken up by macrophages and pass through lymphatics to lymphnodes and other tissues (Mycobacterium tuberculosis)
- Cutaneous penetration occurs in skin injury or insect bites
Dissemination
Growth
- It is very important for all bacteria except that grows on food stuffs and produce toxins
- Iron is a limiting nutrient
- Bacterial ability to take away iron binding protein lactoferrin is a factor for virulence of bacteria
- Gastric acidity is restricting factor for bacterial growth
- Very high body temperature as in birds also limits bacterial growth (anthrax)
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Last modified: Tuesday, 20 March 2012, 6:18 AM