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Lecture №

Infections of the
 central nervous
  and locomotor
    systems
Infections of the central nervous system
caused by:
   trauma leading to breach of integuments of
C.N.S.
   via blood from infective focus.
Meningitis inflammation of the membranes
( meninges ) that cover the brain and spinal
cord.
Bacterial meningitis (pyogenic)
More sever than viral type.
Clinical features. Symptoms of sever headache,
fever, vomiting, photophobia and convulsions
leading to unconsciousness.
Signs of meningeal irritation ,i.e. neck and
spinal stiffness, and kernig ‘s sign ( pain and
The common causative agents of bacterial
               meningitis
  Neisseria meningitidis - common in children
and young adults.
  Haemophilus influenzae - meningitis mostly
seen in children between 1 months and 4 years
old.
  Streptococcus pneumoniae – in old patients.
  Mycobacterium tuberculosis.
Meningitis spread quickly in close household
contacts.
Avoiding overcrowding in living and working
conditions.
Chemoprophylaxis with antibiotics e.g.
Rarely causing meningitis organisms:
Listeria monocytogenes, Leptospira interrogans
and Cryptococcus neoformans.
Laboratory diagnosis:
Examination of C.S.F (lumbar puncture).
C.S.F centrifuged and the deposit Gram-stained
and cultured.
Treatment: dictated by the causative organism
and its sensivity; empirical therapy with two or
three antibiotic drugs is given immediately.
Viral meningitis (aseptic meningitis)
  Benign, self-limited, resolves in 1-2 weeks
  and requires only symptomatic treatment.
  The major route of entry are respiratory and
   gastrointestinal tracts and from these ports
  spread to C.N.S by direct migration via
  olfactory nerves or indirectly via blood.
The major causes of viral meningitis ( aseptic
  meningitis) and/or encephalitis
1. Mumps virus 2. Coxsackievirus
3. Herpes simplex virus 4. Adenovirus
5. Measles virus 6. Influenza virus
7. Varicella-zoster virus
Susceptible persons (the most affected) :
  Children
Encephalitis
  Infection of the brain substance and patient
often show signs and symptoms of meningitis
and encephalitis at the same time.
  Occurs after childhood illness such as
measles, chickenpox and rubella, and rarely
after immunization with vaccines such as
pertussis.
  Patients often die or have debilitating
sequelae.
  Very serious disease needs prompt and
intravenous antiviral treatment.
Poliomyelitis
 Caused by poliovirus types 1-3.
 The port of entry – mouth and the virus
 multiply in lymphoid tissue of the pharynx and
 intestine. Then enters the blood stream and
 causes viraemia, spread into C.N.S and
 causes neurological disease.
 The disease is an influenza-like illness, with
 meningitis and encephalitis.
 In some, damage of the anterior horn cells of
 the spinal cord leads to: 1. respiratory failure.
 2. or permanent lower neuron weakness and
 paralytic poliomyelitis. Two types of Polio
Cerebral abscess
  infection reach the brain through blood or by
direct extension of sinus infection caused by
oral bacteria or, rarely, as complication of acute
or chronic dental infection.
  also flow traumatic injury to the maxillofacial
region.
  infection mostly polymicrobial (mixed) -
streptococci, staphylococci, anaerobic cocci
and coliforms.
  treatment is surgical.
Tetanus Clostridium tetani (drum-stick bacillus).
After I.P. (5-15 days) exotoxins cause sever
painful muscle spasm:
masseter muscles - lockjaw
facial muscles – risus sardonicus (facial
grimace)
Extensor muscles - opisthotonos (arched body)
Pathogenesis
Contamination of wound with spores from dust,
soil or rusty objects results in spore
germination and release of tetanospasmin and
tetanolysin.
The bacteria remain localized at the site of
infection, but the exotoxins absorbed at the
motor nerve endings, diffuse towards the
Epidemiology
Main source is animal faeces.
Tetanus is commonly associated with deep
  penetrating wounds, but it can result from
  superficial abrasions e.g. thorn pricks.
Infection of umbilical stump - neonatal tetanus.
Diagnosis
Mainly clinical.
Treatment
1. Supportive: muscle relaxants, sedation and
  artificial ventilation.
2. Antitoxin: I.V in large dose.
3.Antibiotics: penicillin or tetracycline to
  prevent further toxin production.
4. Debridement: excision and cleaning of the
  wound.
Prevention
Active immunization with toxoid in childhood,
  during
the first year of life and before school entry.
Prophylaxis of wounded patients
 If the patient is immune, a booster dose of
toxoid should be given if the primary course
(or booster dose) was given more than 10 years
previously, and human antitetanus
immunoglobulin (ATS) should be given if the
wound is dirty and more than 24 h old.
 If the patient non-immune, human antitetanus
immunoglobulin should be given, followed by a
full course of tetanus toxoid by injection.
 Penicillin – to prevent tetanus and to avoid
pyogenic infection.
 Booster doses of toxoid 10 years after primary
course and again 10 years later maintain
Infection of the locomotor system
            (bones and joints)
Natural defenses
1. macrophages in synovial membranes of
  joints.
2. mononuclear cells, complement and
  lysozyme of synovial fluid.
Acute septic arthritis
Can be caused by S. aureus, H. influenzae, S.
pneumoniae and other streptococci, N.
  gonorrhoeae
and non-sporing anaerobes such as Bacteroids
  spp.
Others infrequent agents are M.tuberculosis,
Acute septic arthritis may result from:
1. Traumatic injury through the joint capsule.
2. Haematogenous spread, usually as a
  complication
of septicaemia.
3. Extension of osteomyelitis or spread of
  infection
from an adjacent septic focus.
4. Infection of joint prosthesis. source of
  infection
for artificial joints may patient, operating team
  or
theatre air.
Clinical features:
Limitation of movement, swelling, redness and
Reactive arthritis
  Acute arthritis mediated by immunological
mechanism.
  Genetic predisposition present.
  Affecting one or more joints.
  Develops 1-4 weeks after infection of genital
(post-sexual reactive arthritis) or
gastrointestinal tract (post-dysenteric arthritis).
  Post-sexual reactive arthritis caused by
Chlamydia trachomatis and almost all patients
are men.
  Post-dysenteric arthritis follow infection with
Salmonella, Shigella, Yersinia or
Campylobacter.
Osteomyelitis
Acute osteomyelitis
• usually occurs in children under 10 years old.
• mostly caused by S. aureus ; H. influenzae, S.
pyogenes, S. pneumoniae, Salmonella,
Brucella, and non-sporing anaerobes.
Chronic osteomyelitis
• common in adults.
• mostly caused by S. aureus. Salmonella,
Brucella, Mycobacterium tuberculosis.
Osteomyelitis of the jaws
• uncommon due to high vascularity of the jaws,
especially maxilla.
• Predisposing factors such as bone disease
such as osteopetrosis, bone tumors and
irradiation.
Laboratory diagnosis
Blood culture, culture of pus from the bony
focus – pus obtained by needle aspiration or by
open surgery and by specimens from the
infective focus e.g. “ cold abscess ” pus in
tuberculosis.
Treatment
THE
END

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Infections of the central nervous and locomotor systems

  • 1. Lecture № Infections of the central nervous and locomotor systems
  • 2. Infections of the central nervous system caused by: trauma leading to breach of integuments of C.N.S. via blood from infective focus. Meningitis inflammation of the membranes ( meninges ) that cover the brain and spinal cord. Bacterial meningitis (pyogenic) More sever than viral type. Clinical features. Symptoms of sever headache, fever, vomiting, photophobia and convulsions leading to unconsciousness. Signs of meningeal irritation ,i.e. neck and spinal stiffness, and kernig ‘s sign ( pain and
  • 3. The common causative agents of bacterial meningitis Neisseria meningitidis - common in children and young adults. Haemophilus influenzae - meningitis mostly seen in children between 1 months and 4 years old. Streptococcus pneumoniae – in old patients. Mycobacterium tuberculosis. Meningitis spread quickly in close household contacts. Avoiding overcrowding in living and working conditions. Chemoprophylaxis with antibiotics e.g.
  • 4. Rarely causing meningitis organisms: Listeria monocytogenes, Leptospira interrogans and Cryptococcus neoformans. Laboratory diagnosis: Examination of C.S.F (lumbar puncture). C.S.F centrifuged and the deposit Gram-stained and cultured. Treatment: dictated by the causative organism and its sensivity; empirical therapy with two or three antibiotic drugs is given immediately.
  • 5. Viral meningitis (aseptic meningitis) Benign, self-limited, resolves in 1-2 weeks and requires only symptomatic treatment. The major route of entry are respiratory and gastrointestinal tracts and from these ports spread to C.N.S by direct migration via olfactory nerves or indirectly via blood. The major causes of viral meningitis ( aseptic meningitis) and/or encephalitis 1. Mumps virus 2. Coxsackievirus 3. Herpes simplex virus 4. Adenovirus 5. Measles virus 6. Influenza virus 7. Varicella-zoster virus Susceptible persons (the most affected) : Children
  • 6. Encephalitis Infection of the brain substance and patient often show signs and symptoms of meningitis and encephalitis at the same time. Occurs after childhood illness such as measles, chickenpox and rubella, and rarely after immunization with vaccines such as pertussis. Patients often die or have debilitating sequelae. Very serious disease needs prompt and intravenous antiviral treatment.
  • 7. Poliomyelitis Caused by poliovirus types 1-3. The port of entry – mouth and the virus multiply in lymphoid tissue of the pharynx and intestine. Then enters the blood stream and causes viraemia, spread into C.N.S and causes neurological disease. The disease is an influenza-like illness, with meningitis and encephalitis. In some, damage of the anterior horn cells of the spinal cord leads to: 1. respiratory failure. 2. or permanent lower neuron weakness and paralytic poliomyelitis. Two types of Polio
  • 8. Cerebral abscess infection reach the brain through blood or by direct extension of sinus infection caused by oral bacteria or, rarely, as complication of acute or chronic dental infection. also flow traumatic injury to the maxillofacial region. infection mostly polymicrobial (mixed) - streptococci, staphylococci, anaerobic cocci and coliforms. treatment is surgical.
  • 9. Tetanus Clostridium tetani (drum-stick bacillus). After I.P. (5-15 days) exotoxins cause sever painful muscle spasm: masseter muscles - lockjaw facial muscles – risus sardonicus (facial grimace) Extensor muscles - opisthotonos (arched body) Pathogenesis Contamination of wound with spores from dust, soil or rusty objects results in spore germination and release of tetanospasmin and tetanolysin. The bacteria remain localized at the site of infection, but the exotoxins absorbed at the motor nerve endings, diffuse towards the
  • 10. Epidemiology Main source is animal faeces. Tetanus is commonly associated with deep penetrating wounds, but it can result from superficial abrasions e.g. thorn pricks. Infection of umbilical stump - neonatal tetanus. Diagnosis Mainly clinical. Treatment 1. Supportive: muscle relaxants, sedation and artificial ventilation. 2. Antitoxin: I.V in large dose. 3.Antibiotics: penicillin or tetracycline to prevent further toxin production. 4. Debridement: excision and cleaning of the wound.
  • 11. Prevention Active immunization with toxoid in childhood, during the first year of life and before school entry.
  • 12. Prophylaxis of wounded patients  If the patient is immune, a booster dose of toxoid should be given if the primary course (or booster dose) was given more than 10 years previously, and human antitetanus immunoglobulin (ATS) should be given if the wound is dirty and more than 24 h old.  If the patient non-immune, human antitetanus immunoglobulin should be given, followed by a full course of tetanus toxoid by injection.  Penicillin – to prevent tetanus and to avoid pyogenic infection.  Booster doses of toxoid 10 years after primary course and again 10 years later maintain
  • 13. Infection of the locomotor system (bones and joints) Natural defenses 1. macrophages in synovial membranes of joints. 2. mononuclear cells, complement and lysozyme of synovial fluid. Acute septic arthritis Can be caused by S. aureus, H. influenzae, S. pneumoniae and other streptococci, N. gonorrhoeae and non-sporing anaerobes such as Bacteroids spp. Others infrequent agents are M.tuberculosis,
  • 14. Acute septic arthritis may result from: 1. Traumatic injury through the joint capsule. 2. Haematogenous spread, usually as a complication of septicaemia. 3. Extension of osteomyelitis or spread of infection from an adjacent septic focus. 4. Infection of joint prosthesis. source of infection for artificial joints may patient, operating team or theatre air. Clinical features: Limitation of movement, swelling, redness and
  • 15. Reactive arthritis Acute arthritis mediated by immunological mechanism. Genetic predisposition present. Affecting one or more joints. Develops 1-4 weeks after infection of genital (post-sexual reactive arthritis) or gastrointestinal tract (post-dysenteric arthritis). Post-sexual reactive arthritis caused by Chlamydia trachomatis and almost all patients are men. Post-dysenteric arthritis follow infection with Salmonella, Shigella, Yersinia or Campylobacter.
  • 16. Osteomyelitis Acute osteomyelitis • usually occurs in children under 10 years old. • mostly caused by S. aureus ; H. influenzae, S. pyogenes, S. pneumoniae, Salmonella, Brucella, and non-sporing anaerobes. Chronic osteomyelitis • common in adults. • mostly caused by S. aureus. Salmonella, Brucella, Mycobacterium tuberculosis.
  • 17. Osteomyelitis of the jaws • uncommon due to high vascularity of the jaws, especially maxilla. • Predisposing factors such as bone disease such as osteopetrosis, bone tumors and irradiation. Laboratory diagnosis Blood culture, culture of pus from the bony focus – pus obtained by needle aspiration or by open surgery and by specimens from the infective focus e.g. “ cold abscess ” pus in tuberculosis. Treatment