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Name- Corynebacterium diphtheria
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Lesion - Psedomembranous lesion, tightly adhered to the underlying tissue, does not produce any secretions
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Toxin- may or may not produce a toxin- laboratory investigations are hence essential. The toxin attacks cardiac myocytes and prevents protein synthesis within these cells causing infected people to die of cardiac failure
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Vaccine- toxoid vaccine which produces no infection but effective due to inflammatory response generated by host (Infection control measure)
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Treatment- Antibiotic(Penicillin G)+Antitoxin
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Location- upper respiratory tract (if occurs on the vocal cords, it will obstruct the air pathway and can cause death due to asphyxation)
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Caused by Pseudomonas aeruginosa
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Etiology: 80% idiopathic; 80% of the remaining 20% is caused by viral manifestation and the remaining 20% is caused by bacteria
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Bacterial cause: usually Group A Streptococci (Streptococcus pyogenes).
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Streptococcus Pyogenes (group A strep) can have 2 manifestations when they enter a host:
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1. Infectious Diseases
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Scarlet fever, Erysipelas, Necrotizing fasciitis (tissue necrosis)
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2. Post Infectious Diseases / Inflammatory diseases
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Rheumatic Fever, Post infection Glomerulonephritis
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1. Rheumatic Fever
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permanent condition and eventually requires valve replacement
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Mechanism:
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Molecular Mimicry
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2. Poststreptococcal Glomerulonephritis
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temporary and resolves without long lasting damage
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Mechanism:
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Complement Activation
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M protein is a sequence of amino acids present on the bacteria and also present on the cells of the heart. This bacterial M protein is the target of the host immune system. however ~20 days post infection, the host's immune cells attack their own body i.e the M cells of the heart. This is called molecular mimicry and involves cross reactive antibodies (attack foreign and later self).
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Molecular mimicry often leads to post-infection manifestations such as Rheumatic Fever
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Rheumatic fever is an example of a post-infectious disease (due to the response of the inflammatory cells on self) that can develop as a complication of inadequately treated strep throat or scarlet fever.
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Rheumatic Fever is characterised by transient arthiritis
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It damages the heart valves and increases the rigidity of chorda tendinae causing mitral insufficiency
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(Complement Activation)
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this disorder produces proteins that have affinity for sites in the glomerulus. As soon as binding occurs to the glomerulus, complememtn is activated. Activation of complement causes generation of inflammatory mediators. Immune complexes are trapped in a subepithelial pattern.
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If blood culture involves Anti Streptolysin O and Anti DNAase B then antibodies should be checked again and again as the child is suspecte of having a streptococcus infection which may lead to greater complications
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If culture for Group A,C and G is negative for a case of repetitive/recurring pharyngotonsillitis wherein the patient presents with fever, this bacteria must be considered because it has serious implications
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Manifestations:
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pharyngitis, osteomyelitis, sepsis, invasive infections
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Cause
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due to use of internal tampons
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Signs:
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Hypotension, Fever >38.5, Rash, Renal Impairment, Coagulopathy /DIC Alteration liver enzymes, Acute Respiratory Distress Syndrome (ARDS), Tissue necrosis (necrotizing fasciitis)
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Clinical presentation
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unilateral sore throat that increases in intensity over several days with earache, a bad taste and fetid breath
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Pathology
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necrotising infection of pharynx
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Cause
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combination of Fusiform bacteria and Spirochetes
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Manifestation
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deep well circumscribed unilateral ulcer of one tonsil. The base of the ulcer is gray and bleeds easily when scraped with a swab. There may be submandibular lymphadenopathy.
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Treatment
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Penicillin or Clindamycin and surgical debridement
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Interesting cheat sheet. I'd suggest you to add more tags such as 'oral', or 'pathology' so students like I could find it with ease. Greetings!
Cheatography n. The art of mapping complex subjects into clear, instantly navigable reference guides.
