Infections transmitted by direct physical contact - anthrax, tetanus, rabies. Organ site pathomorphology
Anthrax
An infection caused by Bacillus anthracis. Can occur in skin, lung, intestinal or injection forms. Symptoms occur within a month. Anthrax is spread via bacterium’s spores which can be breathed in, consumed or come in through broken skin. Use of anthrax as a weapon is the greatest risk, although it is common in Africa and central and southern asia.
The pathogenesis is thanks to the two virulence factors of poly-D-glutamic acid capsule which prevents phagocytosis and the anthrax toxin (contains protective antigen, edema factor and lethal factor).
Skin form symptoms
- Most common form, least dangerous
- Causes a boil-like skin lesion that ulcerates with black center (necrotic region)
- After time begins to blister, surrounding area we can see cellulitis with marked edema
Lung form symptoms
- Affects lymph nodes in lungs first, causing hemorrhagic mediastinitis with bloody fluid accumulating in mediastinum leading to shortness of breath
- First stage of disease involves flu-like symptoms
- Second stage (from here 90% fatal) pneumonia occurs as infection spread from lymph to lungs
GI form symptoms
- Occasional vomiting of blood can occur, with lesions in intestines, mouth and esophagus.
- Bacteria can spread to bloodstream and become systemic
- This is the rarest form of anthrax
Tetanus
Tetanus is a bacterial infection of Clostridium tetani characterised by muscle spasms due to a neurotoxin. C.tetani spores are found commonly in the environment (dirt etc) and as the bacteria are anaerobic they thrive in wounds. Tetanus affects skeletal muscle only the tetanus toxin binds to nerve terminals in the periphery and travels to the CNS where it fixes to gangliosides at the presynaptic inhibitory motor nerve endings, where it goes to block the release of GABA and glycine (inhibitors) across the cleft, causing nerve impulses and muscle spasms.
Memory aid: tetanus vs botulism - tetanus toxin blocks the inhibitory transmitters (glycine and GABA) of spinal interneurons, so muscles cannot relax: spastic paralysis (lockjaw, risus sardonicus, opisthotonus). Botulinum toxin blocks acetylcholine release at the neuromuscular junction: flaccid paralysis.
Symptoms begin with lockjaw, with chest, neck, back, abdominal muscles all to follow. Prolonged muscular action can cause groups of muscle to spasm, known as tetanic spasms. Other systemic symptoms of bacterial infection also occur (note tetanus has an incubation period of usually about 10 days).