2024 Dina Filariasis and toxoplasmosis.pdf

Microbiology

1. Lymphatic Filariasis
Presented by
Professor Dina Abou Rayia
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2. Filariae affecting the lymphatic
system
1.Wuchereriabancrofti(Africa, Asia and America)
2.Brugiamalayi(Southeast Asia)
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3. Lymphatic Filariasis
Wuchereriabancrofti
Geographical distribution
1.Tropicalandsubtropicalregions(West&CentralAfrica,SouthAmerica).
Habitat
Lymphatic system especially that of lower limbs
D.H Man
I.H (vector) Mosquitoes (Culex, Anopheles, and Aedes).
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4. Morphological characters
Adult
Longthreadlike.
Femaledepositslarvae
calledmicrofilaria.
Male(4cm)isshorter
thanfemale(8-10cm).
Adultshavecylindrical
esophagus
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5. Microfilaria (D.S)
Microfilariais250μmx8μm,bodywithsmoothcurves,
loosesheathwithdeeplystainednucleiwithemptyant.
andpost.ends&havenocturnalperiodicity(10p.m.to2
a.m.).
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6. Mosquito ingests
microfilaria with blood
Microfilariae penetrate
stomach to thoracic muscle
Microfilariae metamorphose
after 2 molts L3
L3 migrate to proboscis &
drop on skin during biting
Infective (L3) enter
through mosquito bite
L3 molt twice &
adults appear in
lymphatics after
6-12 Ms
Adults in lymphatics
Females Lay microfilariae
in lymphatics
Mosquito
I.H.
Human
D.H.
microfilariae appear in
peripheral blood at night
Life cycle of lymphatic filariasis
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7. 7

8. Mode of infection
Mosquitobitestheskinforbloodmealthenthe
infectivestage(3
rd
stagefilariformlarva)inthemouth
partisinoculatedintheskinthroughthebitewound.
Diagnostic Stage
Loosely sheathed microfilaria in the peripheral blood at
night.
Infective stage
Third stage filariform larva
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9. Pathogenesis and symptomatology
Disease:Bancroftianfilariasisorelephantiasis.
Pathologicallesionsoccurinthelymphaticsystem,
duetothepresenceofadultworms(livingordead)
butnotduetomicrofilariae.
Occursinendemicareaswherepatientsremain
asymptomaticbutwithpatentmicrofilariaintheir
blood.
1. Asymptomatic phase:
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10. 2-Acute inflammatory phase
Recurrent attacks of lymphangitisand lymphadenitis due to
Toxic
productsof
livingordead
adultworm
Mechanical
irritation by
adult worm
Allergicreactionto
adultproductsor
diedworms
2
ry
bacterial
infection
Symptoms
fever, chills
& headache
Local lymphangitis Lymphadenitis Affection of
lymphaticsof
epididymisand testes
(epididimo-orchitis)
Scrotaum
(varicocoele & hydrocoele)
spermatic cord
(funiculitis)
Vulva
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11. 3-Obstructive (chronic)phase
The obstruction of lymph flow is due to
Blockage of
the lumen
by worms.
Proliferation of
the endothelial
lining
Fibrosis & stenosis
of lymph vessels
Fibrosis of lymph
nodes draining
the area.
Effects of obstruction
The lymph
vessels
become
dilated,
distended
&varicosed
Oedema
Rupture of distended
vessels
Elephantiasis
In renal pelvis or
urinary bladder
Chyluria
(milky urine)
In pleural
sac 
chylothorax
Peritoneal
sac chylous
ascitis
Tonica
vaginalis
of testis 
chylocele
Intestine
chylous
diarrhea
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12. Elephantiasis
•Itoccursafteralongduration(5-10years).
•Itisusuallyaffectedmostdependentpartse.g:Legs,scrotum,&vulva.
•Bloodsampleisnegativeformicrofilaria.
Presented by
Exessiveprotein in
lymph exudate
stimulates
proliferation of fibrous
connective tissue
thickening of the
affected part.
The skin and underlying
tissue become hard,
dense, cracked and non
pitting with loss of
elasticity.
The skin appears
rough, folded,
stretched &fissured
2
nd
bacteria and
fungal infection.
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13. 13

14. 4-Tropical pulmonary eosinophilia
(Occult filariasis)
1.Occursinendemicareasoffilariasisduetoimmunologic
hyperresponsivenesstomicrofilaria.
2.Noclassicallymphaticpathologyandnomicrofilariainthe
blood.
3.Themicrofilariaeareseeninthelungtissues.
4.Scatteredlungopacitieswithasthmaticcoughandwheeze.
5.MarkedeosinophiliawithhighIgElevelsandhighantifilarial
antibodytiter.
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15. Laboratory Diagnosis
Blood
examination
for
microfilariae
Examination of
urine (chyluria) for
microfilaria
Aspiration of
lymph nodes or
hydrocele.
X-ray
for calcified adult.
Immunodiagnosis
Eosinophilia
PCR
Wet mount
preparation
Stained thin &
thick blood films
by Giemsa&
Leishman
Concentration
techniques:
-Knott’s method
-Membrane
filtration
Diethylcarbamazine
(Hetrazan)
Provocation test
Skin test &
serological
testes
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16. Treatment
Early cases Late cases
1)Diethylcarbamazine (Hetrazan)
mainly against microfilariae
2) Ivermectinthe same use as
DEC but single dose
3) Albendazoleeffective againat
adults
4) Corticosteroids
Surgical treatment
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17. Toxoplasma gondii
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18. Habitat:intracellular in any tissue cells of the host except mature RBCs.
Morphology:
•Trophozoite:Crescentic, 5x3 µ with one pole more rounded.
•Oocyst: derived from cat 10x12 µm (disporocystictetrazoic)
•Pseudocyst: without true cyst wall and the host cell contains rapidly
dividing tachyzoites
•True cyst: with true cyst wall and slowly dividing
bradyzoites
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19. 19

20. Sexual enteric
cycle in D.H
Schizogony
&
Gametogony
Immature
oocysts pass
with faeces
Sporozoitesrelease in
intestine
Multiply in lymphoidsof intestine
Spread to various organs
Pseudocystsand cysts are
formed
Mature within 3-4 days
Infective to all hosts by
ingestion
Asexual
exoentericcycle in
I.H
Congenital
infection of the
foetus by
trophozoites
Infective to all hosts by
ingestion
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21. Modes of infection
whenthemother
isinfectedforthe
1
st
timeduring
pregnancy.
(2)-Acquired
(1)-Congenital
(transplacental)
Ingestion of
undercooked
meat with
pseudocysts
and cysts
e.g. beef,
pork and
lamb.
Ingestion
of oocyst
in food
and drink
directly
or
indirectly
by flies.
Inhalation
of
oocysts
with dust
infected
with cat
faeces
Blood
transfusion
&tissue
transplants
Laboratory
exposure to
infection
with
trophozoites
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22. (A)-Congenital toxoplasmosis
If the mother is
infected
before
pregnancy
If the mother is
infected in the 1
st
or
the 2
nd
trimesters
for the 1
st
time
If the mother is
infected in the
last trimester
for the 1
st
time
Shewilldevelop
antibodies(IgG)
thatcrossthe
placenta and
protectthebaby
againstinfection.
Abortionorstillbirth
(borndead)occurs.
The baby will be born
with congenital
anomalies as:
1-Hydrocephalus.
2-Microcephalus.
3-Encephalitis.
4-Cerebral calcification
5-Mental retardation.
6-Chorioretinitis.
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23. 23

24. (B)-Acquired toxoplasmosis
Immunocompetent patient Immunocompromised patient
Glandularformwith
feverandenlarged
liver,spleenandlymph
nodesandsorethroat.
Acuteexanthematous
formwithhighfever,
skinrashandL.N
enlargement.
Latentcysts:inthe
eye,brainandmuscles
which are
asymptomatic
Iftheimmunesystem
issuppressed,dormant
cystbecomereactivated
resultinginflareup&
possiblydissemination
of the infection
(Reactivation).
Mostcasespresent
withCNSmanifestations
(encephalitis, brain
abscess,meningitis),
myocarditis&pneumonia
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25. Laboratory diagnosis
Direct methods Indirect methods
Examination of
biopsy from
enlarged lymph
nodes.
Samples from
blood,CFSorbone
marrow
Immunodiagnosis PCR
CT scan
& X ray
1-I.D.test(toxoplasmin,Frenkel
test).
2-Serologicaltests(forIgG&
IgM):CFT,IHAT,ELISA,IFAT
3-AntigendetectionbyELISA
4-Sabin-Feldmandyetest
(failureoftrophozoitestostain
withmethyleneblueinthe
presenceoftheantibodies)
IgG avidity test
????
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26. Treatment
(1)-Combinationofpyrimethamine(Daraprim)+
sulphadiazine+Folicacid.
(2)-Spiramycinusedmostoftenforpregnantwomento
preventtheinfectionoftheirchild.
(4)-Laserorcryotherapyforchorioretinitis.
(5)-Systemiccorticosteroids.
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27. 27

28. •Wuchereriabancroftiinfection could be
transmitted by blood transfusion ???? Why ???
•Toxoplasma gondii could be transmitted by
autoinfection ??? Why????
•Though Toxoplasmais widespread in nature the
disease is rare???
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