TropMed 2

Malaria : Alterations of the host cells: 1. A visible change of shape and reduced
deformability 2. The presence of electron- dense protrusion/knobs 3. Small
depression/caveolae at the surface pf RBC connected by a network of small
vesicles and clefts in P.vivax and P.ovale 4. Cytoadherence to endothelial cells 5.
Adherence to N erythrocyte : rosetting ; to infected erythrocyte : clumping 6.
Presence of new metabolic channels --) increased membrane permeability,
increased intake of nutrients, or escape from immunity by sequestration.
Pathogenesis : asexual stages(Gametocytes not involve in pathogenesis)
Pathology : -Hemolysis : direct invasion & rupture of RBC during erythrocytic
cycle ; Increased osmotic fragility of RBC
-Increased adhesiveness of
infected RBC: increased with maturity of parasite (schizont>trophozoite) ; Knob
theory -Release of pyrogens, toxin and cytokines -Immunological responses
-Capillary permeability -Tissue hypoxia
Pathogenesis : -Cytoadherence -infected RBCs will adhere to the endothelium as
well as to each other -High cytokine levels induce expression of endothelial
adhesions: inflammation makes the endothelial sticker -Cytokines can mimic
many of the symptoms of malaria : shivering,headache, chills, spiking of
fever,sweating,vasodilation,hypoglycemia -Adherence and Inflammation
reinforce each other in an unholy circle causing pathology 0
Immunity influenced by : genetics, age, health condition, pregnancy status,
intensity of transmission in region, length of exposure, maintenance of exposure
Immunity : Innate :: Red cell polymorphism associated with some protection -) Hb
S sickle cell -)Hb C and E -) Thalassemia a and B -) G6PD
Red cell membrane
changes : absence of certain Duffy coat antigens improve resistance to P vivax
: Acquired ::
Transferred from mother to child -) 3-6mos protection -) Then the children have
increased susceptibility
Increased susceptibility during early childhood : Hyper and holoendemic areas -)
By age 5 attacks usually < frequent and severe -) can have >parasite densities
with fewer sx :Meso - or hypoendemic areas : less transmission and repeated
attacks May acquired partial immunity and be at higher risk for symptomatic
disease as adults
No complete immunity :can be parasitemic without clinical disease
Need long period of exposure for induction May need continued exposure for
maintenance
Immunity can be unstable :can wane as one spends time outside endemic area
can change with movement to area with different endemicity decreases during
pregnancy,risk improves with increasing gravidity
Immune mechanisms :
Anti sporozoite antibodies in adults in endemic areas -) blocks liver invasion
Anti sporozoite/merozoite antibodies -) block RBC invasion

Cytokines : TNF block merozoite development ;IL1 Il10

Erythrocyte clearance : liver and spleen -) block cytoadherence Enhance
clearance through opsonisation ADCC likely Nk activity

Wuchereria bancrofti
Culex ,Anopheles, Aedes
F>M (>Brugia malayi)
(rambut)

Cephalic : L=W
Inti : teratur
Ekor: runcing inti-ve
Badan : smooth
Tungkai atas dan bawah
(termasuk paha)
Genital(dancing worm on
usg)
Mammae
Stadium Inflammation :
Fever, Lymphangitis,
Lymphadenitis
Stadium Obstruction :
Lymph varices on axillae,
inguinal, gnital,
hydrocele
Microfilaria ob blood
film : Giemsa, H&E.
Centrifugation of blood
dissolve in Formalin2%
(Knott) / filtration through
nucleopore membrane
Antigen :
Immunochromatographic
test(only W bancrofti)
Biopsy PCR

mosquitoes
Cacing dewasa -hidup di
Lymph
*ingest L3 larvae to a
person
Microfilaria (d) (Nocturnal
Period : 10pm-2am)

Elephantiasis (end stage)

(adult worm die in
Lymph)

Clinical Manifestation

Diagnosis

Brugia malayi
Mansonia(desa),
Anopheles(kota)
(F>M) <W bancrofti (white
thread)

Cephalic : l=2W
Inti : kasar x teratur
Ekor : runcing 2inti
Badan : patah-patah
Below the knee
scrotal

Almost same as W bancrofti

Tropical Pulmonary
Eosinophilia syndrome :
nocturnal cough, wheezing,
fever,eosinophilia
Xray : nodule, Interstitial
thickening
Same except antigen
detection

DEC(diethylcarbamazapi
ne)
short-term : 5mg/BW
->6d
Long-term : 3-4mg/BW
->10d
Elephantiasis :
compression
surgery(shunt
nodovenous) , raise the
leg up, stocking, leg
treatment

Treatment
*DEC prophylaxis6mg/bw/day for 2d
monthly

1)DEC+Ivermectin(no
microfilariacidal effect)
: 6mg/bw/24h for 12d or
divided dose : 1st-3rd (13mg/Bw/24h
4th-12th(13mg/bw/12h)
2)Albendazole(400
microgr/bw)
+ Ivermectin
3)Albendazole +DEC

Classification :
Grade I : pitting edema + , dismiss spontaneously by applying pressure
Grade II : non pitting edema, not affected by pressure applied
Grade III (elephantiasis) : Grade II + dermatosclerosis + papilomatous

TORCH (Toxoplasmosis, others Rubella, Cytomegalovirus, Herpes)

Toxoplasmosis

Rubella

Cytomegalovir
us

Herpes

-Protozoa Toxoplasma gondii

Transmission :
a.Ingestion of T eggs from
soil *
b. Ingestion of raw or
partially cooked meat *Tissue
cyst containing bradyzoites
c.Contact with infected cat
feces *oocyst containing
sporozoite in cat feces :
ingest unwashed vege
d. Transplacentally(if new
infection occurs during
pregnancy)
e. Through organ transplant
or transfusion-rare
*Tachyzoite widely spread to
eye,brain
Congenital Toxoplasmosis
(cT)
1.When a pregnant woman
gets the infection during
pregnancy and passes it on
her fetus.
2. Women who get
toxoplasmosis Before
conception hardly ever pass
the infection during
pregnancy!!!!!
3.Babies that get infected
during the 1st trimester -most
severe sx
4.40% of foetuses will be
infected when primary
maternal infection
develops at <20wks
gestation

-German measles
family:Toga
Genus:rubivirus
Transmission :
a.Incubation : 23wks
b.Highly
contagious
c.Spread through
naso secrection
d.Transplacental
tx likely
Physical: 3d rash,
swollen grand,
low-grade fever,
joint pain,LOA
Rubella effects:
A.Maternal:
miscarriage and
stillbirth. The risk
of congenital
rubella > 1st
trimester
B. Neonatal :
Cataract, Cardiac
abnormalities,
Deafness, mental
retardation,
movement
disorder,
balancing
problem,
blueberry muffin
spots

Diagnosis : Amniocentesis
-PCR, Ultrasound measure
the level of antibodies

Diagnosis of
Congenital RS :
IgM in
newborn*IgM x
cross placenta

Manifestation of cT :
Hepatosplenomegaly
Chorioretinitis
CNS injury : CT scan with

Prevention ; MMRaround 1yr(before

pregnancy,
conception after

In herpes
family HHV5
Transmission :
a.
Transplacentall
y
b.Human milk
c.Blood
transfusion or
organ
transplant
d. urine or
saliva
CMV effects:
A. Maternal :
mostly
asymptomatic
B. Neonatal :
Jaundice,
petechiae,
hepatosplenom
egaly,
microcephaly,
chorioretinitis
sequelae :
Sezuire,
chorioretinitis,
periventricular
calcification,
Sensorineural
deafness,
motor deficit
5-7% of
newborns with
asymptomatic
congenital CMV
develop
neurological
sequelae(heari
ng loss>)
Diagnosis:
Isolation of
virus from
urine,saliva,
CSF, blood in

HHV2 or HSV2
Transmission:
a.Maternal
genital
b.Ascending
infection if
ROM
*Postnatal
:HSV1 :herpetic
whitlow
Risk:
premature,ROM
>6h, fetal scalp
monitoring
Congenital HSV
Skin vesicles,
Chorioretinitis,
Microcephaly,
Microophthalmi
a, IUGR
1.Skin,Eye,Mou
th
-1st-2nd week
presentation
-Limited to
skin,eye,mouth
/mucous
membrane
-Neurologic
sequelae
Ophthalmology
involved
2.CNS
-Early - 3rd
week
Encephalitis(te
mporal)
3.Disseminated
Hepatitis,
Pneumonitis,DI
C

multiple intracranial,
calcification Hydrocephaly
Seizure Cerebral palsy
Mental retardation
Jaundice
Premature birth or stillbirth
Manifestation of T in human :
-Most are asymptomatic,
mimic mononucleosis
-Acute T: Influenza-like
symptoms, Swollen lymph
nodes, Muscle aches
latent T : bradyzoite forming
cyst in muscle and nervous
Cutaneous and Psychiatric
Diagnosis : may be difficult,
trial of therapy
with(Pyri,sulfa,leuco),
Serology : IgG IgM
Treatment :
1.Infected women :
Fetal infection not confirmed
yet: Spiramycin(1st
trimester): reduce
transmission
Fetus infected confirmed:
3 weeks :Pyrimethamine
1x50mg PO
Sulfadiazine 3x1gr
Alternating 3wks: Spiramycin
3x1gr
until delivery
2.Newborn :
Pyrimethamine 1mg/kg/day
for2-6months --> 1mg/kg
complete 1 yr
Sulfadiazine: 50mg/kg BID
-1yr
Leucovorine: 10mg every
3x/wks, to prevent toxicity of
P

28d of vaccinated,
avoid contact with
rubella ppl)

the first 21d

PCR CMV IgM
immunoblot
Treatment :
IV Ganciclovir

Vaginal
delivery risk in
mom with
herpes:
1st
symptomatic
lesion>
asymptomatic
but newly
infected>
recurrent> past
history
Diagnosis :
Culture :
Mouth>eyes,
skin
Culture:
stool,urine,CSF
DFA
PCR :
Diss>CNS>SE
M
Treatment :
Acyclovir
SEM:
60mg/kg/8h for
14d
Dissem and
CNS:
60mg/kg/8h for
21d

*remember, immunocompromised state may reactivate latent Toxoplasmosis and

results in Congenital Toxoplasmosis
*The most common SE of Pyremethamine : Neutropenia G6PD has to be
screened prior to initiate Sulfadiazine
*Rubella is a mild childhood illness that can pose a serious threat to the fetus, if
a mother contracts during pregnancy
Leptospirosis : Spirochete,family Trepanometaceae L interrogan(pathogen), L
biflexa(saprophyte) hooked end +flagella, examine under dark field. Renal
failure--)most common causes of death.
Mild : flu like syndrome,myalgia, headache Doxycycline 100mg/12h Ampicillin
500-750/6h Amoxycillin500mg/6h
Moderate/severe : icterus,RF,
hemorrhagic IV Penicillin G, Ampicillin, Cetriaxone, Cefotaxime, Erythromycin.
Prophylaxis : Doxycycline 200mg/wk
After an incubation of 2-20d there is
abrupt fever, myalgia/myositis, cough, chest pain hemoptysis -- then recovery
or jaundice, meningitis, uveitis, and RF.
Weils Disease : Icterus, RF,
Hemorrhagic(conjunctiva bleeding + injection : patognomonic)
Varicella : Varicella Zoster Virus (VZV) 5-9yo Respiratory secretion/ fomites from
vesicles or pustule
IP : 14-16d
Day2-4 : Virus replication in regional lymph nodes
Day 4-6: Primary viremia Subsequent second round of viral replication in liver and
spleen Secondary viremia : infection of the skin and appearance of rash by day 14-16 .
Tx : Acyclovir 20mg/kgBB/6h for 5d Preventive : Zoster Immunoglobulin/IM within 72h to
immunocompromized
Herpes Zoster : VZV travels to dorsal root ganglion and become latent Reactivation
occurs with decreased cell mediated immunity
Presence of lesions in all stages in any
one general anatomical area : macules, papules, vesicles, pustules, and crust are located
in proximity to each other. Characteristic : A rapid evolution of macule
papulevesiclepustulecrust The presence of lesions stages in one anatomical area
Chickenpox
14-21d incubation
Mild to no preceding illness
Lesion mostly on trunk
Palms and sole are spared
Lesions at varying stages of development
Scab form 4-7d after rash appears
Vesicles do collapse on punture

Smallpox
7-17d incubation
Fever, severe systemic sx preceded rash by
2-3days
Lesions mostly on face, arms, legs
Palms and soles involved
Lesions at same stage of development
Scabs form 10-14d after rash appear
Vesicles do not collapse on puncture

Hand Foot Mouth disease : coxsackievirus 16 and enterovirus 17

direct contact
with nose and throat discharge, saliva, fluid from blisters or stool of an infected person.
Incubation period : 3-7d Most often children <10yo. Clinical : Non tender macular or
vesicular lesion 4-8mm across tongue and buccal mucosa Rash usually develops 1 d
after mouth lesions. The rash lasts for 1 week and can be tender vesicular,
maculopapular or pustular on the hand, feet, buttock D: clinical
Mental disorder due to Infection
DSM-IV : due to to substitute the terms organic and non organic. 1. Primary mental
disorder and 2.mental disorder due to general mental condition. Evidence of

physiological cause : presence of general medical condition, temporal association,

atypical features
1. Delirium : Fluctuating manner(hours or days), Lab : Electroencephalogram
demonstrates non focal background slowing Tx : High potency antipsychotic agent : low
dosage of Haloperidol 0,5-1mg PO/IV *avoid benzodiazepine
2. Dementia due to HIV : Encephalopathy in HIV infection is associated with dementia
and is termed AIDS demtia complex, or HIV dementia. Etio : Cholinergic deficit and
inflammatory change & opportunistic lesion of the brain. Clinical : Subcortical dementia.
1. Memory impairment
2. One or more of the following : a. Aphasia b. Agnosia c. disturbance in cognitive
functioning
LAB : MRI : demyelination of subcortical white matter PET : hyperactivity in thalamus
and basal ganglia hypoactivity in temporal lobe
Histopathological : white matter and
subcortical destruction
Tx : Control the viral load !!!
3. Amnestic : inability to learn new information and to recall old information Transient :
<1month Chronic :>1 month
Etio : injury to the brain involved w/ memory : middle
temporal(hippocampus mammilary bodies) The afflicted invidual confabulate, that is
create imagined experiences to fill in gaps in memory, confabulated stories tend to be
variable
LAB : Brain imaging : atrophy or enlargement of 3 ventricle or lateral horn
4. Mood disorder : depressive, manic or mixed etio : HIV infection or Interferon for HIV
prognosis is best correction of underlying disease first
5. Psychotic disorder : delusion: somatic, paranoid, religious or grandious or hallucination
: visual, olfactory, gustatory,tactile or auditory Etio : HIV
6. Catatonic : etio: infection No specific lab test Correct underlying cause !
7. Personality change due to general medical condition : marked alteration from the
previous personality Etio : Neurological condition : temporal and frontal lobe or
subcortical structure