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7/25/2019 4. Nervous System Infection
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MICROORGANISM
THAT CAUSE NERVOUSSYSTEM INFECTION
MicrobiologyLaboratory
Medical Faculty U
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BACTERIAStreptococcus pneumoniae
Neisseria meningitidis
Haemophilus influenzae
Mycobacterium leprae
Clostridium tetani
Clostridium botulinumListeria monocytogenes
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Mycobacterium leprae
this organisms was described by Hansen in 1873 (9 years
before Koch’s discovery of the tubercle bacillus
it causes leprosy (orbus Hansen! Hansen’s disease"
it has not been cultivated on artificial media (do not fulfill
Koch’s postulate). #t grows only in the footpads of mice!
armadillos! and tissue culture
spread through direct contact for a long time (as it occured
in certain family! firstly it was indicated as hereditary
disease"
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Mycobacterium sp. (acid fast staining$ %&"
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Morphology & Identification
acid fast straight'curved bacilli
acid fast staining single or in groups! forming globi (pac)ets
of cigars" acid fastness less than M.tuberculosis
patients that had been treated! will give beaded appearance morphological inde*! can be used for follow up the
therapy
has a very long generation time! about 1+ daysDiagnosis :• ,- staining of scraping of s)in! nasal mucosa! earlobe s)in
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LEPROMIN Test
,nalog with tuberculin test (s)in test using materialfrom lepromatous nodules"
.urpose $ evaluation of immunity to M.leprae
$ helping to establish the diagnosis $ to )now the result of therapy
$ determine prognosis
• /esult
0epromin test (" cellular immunity good
prognosis good
0epromin test ($" cellular immunity poor
prognosis bad
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Pathogenesis :
,re intracelullar pathogen
2he lesions involve the cooler of the body s)in! nose!
pharyn*! eyes! testicles! superficial nerves
ultiplies in mononuclear phagocytes mainly histocytes
on s)in 4chwan’s cells in nerves! invades cells of the
myelin sheath of the peripheral nervous system
0ong incubation period several months 5 years
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Classification of leprosy:
TT
(2uberculoid
2ype" .aucibacillary (6H
system" acular s)in lesion 2he s)in have lost of
sensation ffectiveness of # /ecovery occurs
spontaneously
LL
(0epromatous
0eprosy"-ultibacillary (6H
system"-:isfiguring nodules
form all over the body
- 0ioned face-:eformation of the
hand ' foot
(mutilation"- 0epromin test
negative
Borderline
BL
(;orderline
0eprosy"
BT
(;orderline
2uberculoid"
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Hypopigmented Macule in
Tuberculoid Leprosy
Arm Nodules in
Lepromatous Leprosy
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Active, neglected nodulousLL lesions on Face (lioned face"
Deformed
foot
Damaged
hands
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Therapy
::4 ( :apsone " first line therapy/ifampin! clofa<imin! minocycline! fluoro=uinolon
Prevention
ase finding
#solation of patients#mmuni<ation
ontact (especially in children" ::4
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Clostridium tetani
• Clostridium tetani, which causes tetanus! is worldwide in the soil and
in the feces of horses and other animals (spore form">• 2he symptom of tetanus are caused by an e*tremely potent
neuroto*in!
tetanospasmin! that is released by the vegetative bacteria> *tremely
small amounts of the to*in can be lethal for human
Morphology and Identification
is an obligately anaerob endospore forming drumstic) appearance ?ram positive rods
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Clostridium tetani !Gra"#tai$%
drumstick appearance
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Pathogenesis
4poreform of C.tetani introduces the (small deep" wound
?ermination of the spores vegetative form produces to*in
(the to*in will reaches the &4! but the bacterias do not spread from
the infection site and there is no inflammation"
2he to*in initially binds to receptors on the presynaptic membranes
of motor neurons to the spinal cord and brain stem
/elease of the inhibitory (glycine and @$aminobutyric acid" is bloc)ed
2he motor neurons are not inhibited muscle spasms spastic paralysis
2he to*in diffuses to terminals of inhibitory cells from the brain stem
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Clinical finding
#ncubation period A$B days to as many wee)s haracteri<ed tonic contraction of voluntary muscles
$ trismus! loc)Caw (the mouth can not be opened"
$ gradually! other voluntary muscle involved! resulting in generali<ed
tonic spasms (opisthotonus" $ any e*ternal stimulus may precipitate the spasms 2he patient fully conscious and pain may be intense
2reatment of tetanus are not satisfactory prevention is important
.revention (1" active immuni<ation(+" proper care of wounds contaminated with soil! etc>
(3" prophylactic use of antito*in
(A" administration of penicillin
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(Tortora et al !""#$
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Clostridium botulinum can release a very poisonous to*in inimproperly canned food causes botulism (a form offood poisoning"
-irst described as a clinical disease in the early 18DDs
(botulus E sausages 0atin word"
2he spores are widespread in environment
#n the food with al)alis or neutral condition and wound (atanaerobic condition" spore germination
Clostridium botulinum
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● strict anaerob
F produce neuroto*in (e*oto*in"there are 7 antigenic types (, s'd ?"lethal dose for human G 1 µg ,b is not producedheat labile destroyed at 1DDoresistant to ?#2 en<ymes and easy to be absorbedtarget site neuromuscular Cunction by inhibition of
the release of neurotransmitter (,ch"
muscular paralysis
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Pathogenesis
2o*in in the food
,dsorbed from the gut
;inds to receptors of presynaptic membrane of
motor neurons of the .&4 and cranial nerves
.roteolysis of the target 4&,/ protein in the neurons
#nhibits the release of ,ch at the synaps
.aralysis
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1. Botulism
incubation period 18 5 9 hours symptoms
$ dry mouth! constipation! urine retention (because of
to*in affects ,&4 cholinergic" $ paralysis of ocular! pharin*! larin*! and respiratory muscle therapy ventilation! trivalent antito*in (,!;!"
prevention$ canning food with the correct proccess
$ coo)ing food at 1DDo about 1D minutes $ cans (of food" which is swollen throw away
Clinical Importance
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2. Infant botulism
occurs in baby at 8 wee)s 5 8 months age baby’s feeding contaminated by the m>o>
m>o>multiplying at colon of the baby to*in
symptoms$ acute flaccid paralysis (head! nec)! facial! pharyn*!
e*tremities muscle"
$ death caused by diaphragma paralysis
$ is suspected as a causative agent of 4#:4 (Isudden infantdeath syndromeJ"
therapy antito*in! antimicrobial drug
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Listeria monocytogenes
ause stillbirth and neurological disease in animals long
before it was recogni<ed as causing human disease
*creted in animal feces! it is widely distributed in soil and water #n recent years! listeriosis has changed from a disease of
very limited importance to a maCor concern for the food
industry and health authorities Listeriosis has become the fourth most common cause of
bacterial meningitis
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Morphology and Identification
is a short! ?ram positive! non$spore forming rods has a cell wall surface protein called internalin and ActA
has a tumbling motility at ++$+8o but not at 37o primary culture are done on blood agar small <one hemolysis
around the colonies the motility at /2 hemolysis helping to differentiate listeria from
corynebacterium
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Pathogenesis & Immunity
ontaminated foods (cheese! mil)! vegetables"
?astrointestinal tract
internalin interacts with $cadherin (a receptor on epithelial cells
phagocytosis
phagolysosome
the low pH activatesthe bacteria to produce listeriolysin escape into the cytoplasm
proliferation protein ,ct, induce host cell actin polymeri<ation
push the bacterium to the cell membrane cause formation of
filopods (pseudopodia"
#ngested by adCacent cells! macrophage! and hepatocytes
;acteria can move from cell to cell without being e*posed to ,b!
omplement! or .&
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ell!to!cell spread of L.monocytogenes. &otice that the bacterium
has caused the macrophage on the right! in which it resided ! to form
a pseudopodia that is now engulfed by the o on the left (2ortora et al, +DD9"
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Clinical findings
2wo basic forms
1> arly onset$syndrome (granuloma infantseptica"
$ is the result of infection in utero and is a disseminated form
$ characteri<ed by neonatal sepsis! pustular lesions and granuloma
$ death may be occur before or after delivery +> eningoencephalitis! bacteremia
$ most commonly in adult patient with immunocompromi<ed
Therapy ,mpicillin! rythromycin! and trimethoprime$sulfametho*a<ole ephalosporines fluoro=uinolones are not active against
L.monocytogenes
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VIRUS
.olio virus
/abies virus ,/;#/,0! eg> Lapanese ; encephalitis (L;"
astern e=uine encephalitis ("
6estern e=uine encephalitis (6"
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POLIOVIRUS
• .oliomyelitis is an acute infectious disease destruction of motor neurons in spinal cord result in
flaccid paralysis
Heine edine :isease E #nfantile paralysis E ,cute
anterior poliomyelitis
from ?ree)’s
poli grey! myelos spinal cord! itis inflammation
• Host range human mon)ey
• ,ntigenic types
$ based on neutrali<ing antibody 2ype 1 (type ;runhilde"!
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Pathogenesis
outh is the portal of entry of the vi>• #ncubation period usually 7$1A days (3 5 3B days"
• i> present in the throat stool before onset of illness
mouth
multiplication # oropharyn*! tonsil! lymphnodes of nec)! and .eyer’s patchesviremia
to $% via a&ons of '$% (peripheral nerves s)stem" ( anterior horn cells of the spinal cord are most prominent! posterior horn! gray ganglia! also the brain "
The changes of peripheral nerves * voluntar) muscle(the viruses does not multiply in muscle"
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Clinical %indings
• 2he response ranges
from inapparent infection without symptom to a mild febrile!
and to severe and permanent paralysis
A. Abortive poliomyelitis :$ the most common form minor illnes$ characteri<ed by fever! malaise! drowsiness! nausea! vomiting!
constipation! shore$throat
$ recovers in few daysB. Non-paralytic poliomyelitis (Aseptic meningitis) :$ in addition to the symptom above! the patient has stiffness
pain of the bac) and nec)$ recovery is rapid and complete
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. 'aral)tic poliom)elitis #
$ predominating complaint is flaccid paralysis! usually
unilateral (cause of lower motor neuron damage"
$ recovery usually occurs within months with residual
paralysis lasting much longer
D. 'rogressive postpoliom)elitis muscle atroph) #
$ a result of physiologic and aging changes in paralityc patient
$ although is rare! it is a specific syndrome
• a'oratory Diagnosis
$ spesimen throat swab! rectal swab
$ isolation of vi cell cultures cytopathic effect
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• Immunity
$ permanent to the type causing the infection$ low degree of heterotypic resistance between type 1 +$ the maternal ,bs gradually disappear during the first months of
the baby$ passively administered ,bs lasts only 3 5 B wee)s
• Treatment & Prevention
- symptomatic supplement ( no specific antiviral therapy"
! prevent ion live vi> )illed vi> vaccine are available
e=ually well in preventing paralytic infection
! waste water treatment and sanitation
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%al+ vaccine (+illed vi."
$ from .K cell culture $ periodic booster immuni<ation will be necessary
$ induce humoral immunity! not induce local intestinal immunity
polio vi> still able multiply in the gut
! administered by inCection ( i>m>"
Sabine vaccine (live attenuated-vi.) :
$ from .K human diploid cells
$ oral administration
$ induce humoral local intestinal immunity
$ vi> multiplies! infects in the gut
disseminate the immunity to community
mutation of the vaccine vi paralytic disease (rare"
$ re=uires multiple doses to establish permanent immunity
$ other enteroviruses may be bloc) the immunity
PI )*CCI+,
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RAIES
is a disease that almost always results in fatal encephalitis from 0atin E madness
worldwide! humans usually are infected from the bite of an infected animal 5 especially dog or bats the immune response is ineffective because the viruses in
the wound in numbers too low to provo)e itM also they do not
travel through the bloodstream or lymphatic system
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.athomechanism of rabies infection (2ortora et al! +DD9"
nce the virus enters
the .&4! is not
asccesible to the
immune system until
cells of the nervecells to be destroyed
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Morphology & Identification
• ?enus 0yssavirus
• ss /&,! bullet shaped (7B * 18D nm"
• envelope ("! spi)es ("• intracytoplasmic replication
• rabies virus produces a specific cytoplasmic inclusion
bodies! negri bodies! in infected nerve cells
• released by budding formation
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2he incubation period! may depend on the amount of inoculum
attac)ed tissue
condition of host
distance of the virus has to travel from its point of entry
to the brain
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Clinical %inding
primary infection attac)ed by animal
as an acute encephalitis fulminant! and fatal
3 phases of the disease
1> .rodromal
not specific!+> ,cute neurologic phase catalepsy! hydrophobia
3> omma death!because of respiratory paralysis
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a'oratory Diagnosis
,ntigen detection negri bodies
#solation viral identification
4erology
animal observation (during 1D days" if it has positive sign for encephalitis or abnormally
behaviour )ill the animal! send the head to referrallaboratory (;iofarma $ ;andung"
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Prevention
accination
1> H: (human diploid cell vaccine">
+> &2 (nerve tissue vaccine"! from goat>
3> : (duc) embryo vaccine">
A> 0, (live attenuated vaccine"! from
chic)en embryo
/abies antibody from man or from horse
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To person -ho -as 'itten 'y -ild animal
wash the wound with water and antiseptic! do not be wound toilet
sutured if there is an indication gives rabies antibody antimicrobial agent ,24 prophyla*is animal observation
To animal• vaccination of pet dogs and cats
Control
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&RION#
.rions can cause degenerative &4 diseases
Kuru! L: (reut<feldt$La)ob disease"! bovine spongiform
encephalopathy! scrapie (sheep"! fatal familial insomnia
(human"! transmissible spongiform encephalopathies (24"
,re not conventional viruses infectivity is associated
with proteinaceous material devoid of detectable amountsnucleic acid
,n abnormally folded protein>
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,lthough the etiologic agent may be recoverable from other
organs! the disease are confined to the nervous systemlinical feature
$ neurodegeneration and spongiform changes
$ long incubation periods (months to decades" followed by
chronic progressive disease (wee)s to years"
$ always fatal! with no )nown cases of remission or recovery
$ no inflammatory! no immune response (not antigenic"!
no production of interferon
$ chronic inflammation induced by other factor (viruses!
bacteria! autoimmunity" may affect the prion pathoigenesis
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FUNGI
Cryptococcus neoformans
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CRY&TOCOCCOSIS
,gent Cryptococcus neoformans
Neast cells! O A$ Pm! with thic+ polysaccharides$
glucorono*ylomannan capsules! Q +B PmHabitat soil! bird dropings
aCor clinical findings chronic meningitis! with spontaneous
remissions and e*acerbationsM may resemble brain tumor!
brain abscess
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Cryptococcus neoformansThis yeastlike fungus has an unusually thick capsule.
(suspending the cells in dilute India ink$ (Tortora et al !""#$
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;ilateral patchyinfiltrates
utaneous cryptococcosis
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Diano!i!
4pecimens 4-! sputum! blood! urine:irect e*amination using #ndia in) thic) capsuleulture medium cyclohe*imide4erology
"#erap$,mphotericin ;-lucytosine
-lucona<ole
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