I.
Bacterial
Meningitis
- Meningitis
is an inflammation of the meninges, the membranes that cover the brain and spinal cord
Meninges
(spinal & cranial) –
protective coverings around the brain and spinal cord.
a. dura
mater -
"tough mother;" outermost layer of the meninges; tough, fibrous connective
tissue; gives structural support.
b. arachnoid
mater-
"spider layer;" middle layer of the meninges; weblike appearance; arachnoid
villi capillaries function in the absorption of cerebral spinal fluid (CSF) (CSF is the
fluid that circulates around the brain and spinal cord to provide nutrients and oxygen and
to take waste products away).
d. subarachnoid
space -
between arachnoid & pia mater; where cerebral spinal fluid circulates.
e. pia
mater
- "delicate mother;" innermost layer of the meninges; transparent fibrous
membrane that adheres to the surface of the spinal cord & brain; it contains numerous
blood vessels.
B. Haemophilus
Meningitis
– Hameophilus
influenzae
type B (Hib) causes 2/3 of bacterial meningitis cases during the first year of life;
children can be carriers; human are exposed to bacteria early in life and rapidly acquire
immunity, so disease is rare in adults; almost always fatal if not treated (about 1/3 die
even with treatment); leading cause of mental retardation in US and worldwide; Hib vaccine
has drastically reduced incidence.
C. Streptococcus
Meningitis
– leading cause among adults; organism spread via the blood from lungs, sinuses, and
ear infections.
D. Can
also be caused by E. coli and Staphylococcus species.
B. Encephalitis
The
Disease – Causes an inflammation of the brain. 4
types (all caused by a different virus): Eastern
Equine Encephalitis (EEE), Western Equine Encephalitis (WEE), Venezuelan Equine
Encephalitis (VEE), and St. Louis encephalitis (SLE).
Named because they infect horses more often than humans.
Transmission
– usually from a mosquito to a bird, back to a mosquito, and to a horse, human, or
other mammal.
Clinical
Signs – Fever, headache; convulsions sometimes occur.
EEE is the most serious (causes sever necrotizing infection of the brain). VEE resembles the flu in humans. SLE occurs in late summer epidemics about every 10
years and is severe in elderly patients.
Treatment
only alleviates symptoms. Vaccines are
available for horses, but are not used on humans for fear of inducing a virulent form of
the disease.
Transmission
– bite (viruses are shed in saliva)
Diagnosis
– IFAT (immunofluorescent antibody test) developed in 1958; animal is killed and its
brain is examined for rabies antigens; prior to 1958, brain was examined for Negri bodies (inclusion bodies-clusters of
viruses in neurons).
The
Disease
– virus replicates in injured tissues and then slowly migrates to nerves where it
eventually reaches the central nervous system (brain/spinal cord); the length of time
required for symptoms to appear is proportional to the distance between the wound and the
brain and is affected by the accessibility of nerve fibers (think about a face bite vs. a
foot bite).
Clinical
Signs
– headache, fever, nausea, partial paralysis near the bite site (persist for 2-10
days, then worsen); paralysis then becomes more general, throat muscles undergo painful
spasms, confusion and hallucinations occur; 10-14 days after onset, patient goes into a
coma and dies.
Treatment
– Ordinarily there is sufficient time for the bitten individual to be vaccinated and
to respond by making enough protective antibodies to prevent onset of the disease; once
symptoms have occurred it is too late to vaccinate and death usually follows quickly. No longer administer 20 abdominal injections/day
to treat rabies! The current vaccine is given intramuscularly on days 0, 3, 7, 14, and 28. Hyperimmune globulin (antibody) is also placed
deep in the wound and infiltrated around the wound (remember passive immunization).
A. Hansen’s
Disease – already
discussed
B. Tetanus
–
already discussed
C. Botulism
& Infant Botulism –
already discussed
Prion
Defined: infectious agent composed only of
protein (no DNA or RNA!).
Includes
Kuru and Creutzfeldt-Jakob Disease (CJD) of humans, mad cow disease, scrapie of sheep,
chronic wasting disease of elk and mule deer. These
diseases are referred to collectively as transmissible
spongiform encephalopathies because they give brain tissue a spongy appearance.
Kuru
(“Laughing Death”) – Spread
through breaks in the skin; occurred mainly in New Guinean women. Discovered that they prepared the bodies of the
dead for cannibalistic consumption and smeared their own bodies with the raw flesh of the
corpses. Since cannibalistic rites have been
stopped, the disease has disappeared.
CJD
–
in most cases, no source of prions has been identified; there seems to be a genetic
predisposition in some families.
Mad
Cow Disease
– reached a peak in Britain in the early 1990’s; spread through the practice of
boiling down animal remains for livestock feed. The
US has banned the import of British beef,
cattle, and beef products.
Prions
have clearly been transmitted from one species to another in lab trials.
Could
play a role in Alzheimer’s and Parkinson’s diseases.