INFECTIOUS DISEASES

NADRAH BINTI OTHMAN E5

Toxoplasmosis

others - HIV

rubella
TORCH

herpes simplex

cytomegalovirus

TOXOPLASMOSIS :
Pathophysiology :
Ingesting food contains cysts/contaminated with oocysts usually
from acutely infected cats or may also be transported to food by
flies and cockroaches

Toxoplasma gondii acquired

When organism ingested , bradyzoites are released from cysts or

sporozoites from oocysts

Organism enter gastrointestinal cells where they :

-multiply
-rupture cells
-infect contiguous cells

enter lymphatics

disseminate hematogenously throughout the body

tachyzoites proliferate , producing necrotic foci surrounded by

cellular reaction

normal immune response [both humoral & cell-mediated]

tachyzoites disappear from tissues

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NADRAH BINTI OTHMAN E5

INFECTIOUS DISEASES

*immunocompromised & immunocompetent persons , acute

infection progresses & may cause potentially lethal disease ,
including pneumonitis , myocarditis or encephalitis

effect acute T.gondii infections :

- alterations of T-lymphocyte populations include
lymphocytosis , increased CD8 count , decreased CD4 :
CD8 ratio
*depletion of CD4 cells in AIDS patient may contribute to
severe manifestations of toxoplasmosis

characteristics lymph nodes changes : reactive follicular

hyperplasia with irregular clusters of epitheliod histiocytes
that encroach on and blur margins of germinal centers , and
focal distention of sinuses with monocytoid cells

checkpoint notes :
1. cysts form early as 7 days after infection & remain for the life
of the host
2. latent infection produce little or no inflammatory response
but can cause recrudescent disease in immunocompromised
persons.
Congenital Toxoplasmosis
Mother acquires infection during gestation

Organisms disseminate hematogenously to placenta

Infection may be transmitted to the fetus by :

1.transplacentally
2.during vaginal delivery

untreated maternal infections acquired at :

- 1st trimester >>> 17% with severe disease
rd
- 3 trimester >>> 65% fetus with disease that is mild or
inapparent at birth
*different rates of transmission and outcome related to
placental blood flow , virulence , inoculum of T.gondii &
immunologic capacity of the mother to limit parasitemia
Clinical manifestations :
chronic inflammation and cysts
Wright/Giemsa stain/periodic acid-Schiff/silver
stains/immunoperoxidase technique tachyzoites can be seen
1. Microscopic - area of necrosis may be present in many
tissues especially CNS , choroid and retina , heart , lungs ,
skeletal muscle , liver , and spleen
2. Calcification occur in the brain

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INFECTIOUS DISEASES

Infection in the pregnancy may result in (occur only if there is acute

exacerbation during pregnancy) :

1.
2.
3.
4.

Spontaneous abortion
Perinatal death
Abnormal growth
characteristic triad of fetal anomalies :
chorioretinitis
hydrocephaly / microcephaly
cerebral calcification

RUBELLA :
Pathophysiology :
Rubella virus Infections

Virus replicates in the respiratory epithelium

Spreads to regional lymph nodes

Viremia ensues and most intense from 10-17 days after infection

10 days after infection : viral shedding from the nasopharynx begins and
may be detected up to 2 week following onset of rash
*highest communicability is from 5 days before to 6 days following
appearance rash

Infections during 1st 8 week gestation >>>most severe & widespread

defects

Causes cellular & tissue damage in infected fetus may include tissue
necrosis due to vascular insufficiency , reduced cellular multiplication time
, chromosomal breaks and production of a protein inhibitor causing mitotic
arrest in certain cell types

Virus persists in fetal tissue until well beyond delivery

Possibility ongoing tissue damage & reactivation, most notably in the

brain
Clinical manifestation :
Symptoms: Mild pyrexia, arthralgia, rash which persists for a week and
always affecting the face, lymphadenopathy in the postauricular, deep
cervical and suboccipital L.N. precedes the appearance of the rash and
persists for 3 weeks.
ii.
The congenital rubella syndrome includes :
Neuropathic changes
- microcephaly
- mental & motor retardation
- meningoencephalitis
i.

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INFECTIOUS DISEASES

- cerebral palsy
- cerebral calcification
Cardiovascular lesions
Persistent ducats arteriosis
Pulmonary artery stenosis
Atrioventricular septal defects
Ocular defects
Cataract
Micropthalmia
Retinal changes , retinitis
Blindness
Inner ear problem
Sensorineural
Symmetric intrauterine growth retardation
Other :
Purpura
Jaundice
Hepatoplenomegaly
Thrombocytopeniac

CYTOMEGALOVIRUS :
Pathophysiology :
Transmission of CMV :
- direct: person to person contact ( saliva, milk, urine, semen, tears,
stools, blood, cervical and vag. Secretion.).
- indirect: contaminated fomites.

Cytomegalovirus infections
mostly affected organs :
lung , liver , kidney , gastrointestinal tract , salivary , and other
exocrine glands

CMV induces an inflammatory reaction

Enhances and prolonged by the presence of viral replication

Presence of CMV in areas of inflammation increases the expression of

soluble mediators such as cytokines and chemokines

CMV infects placental cytotrophoblast and can be transmitted to the

fetus

Clinical manifestations :
Complications of fetal CMV infection include:
1. micro-& hydrocephaly
2. chorioretinitis

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3.
4.
5.
6.

INFECTIOUS DISEASES

cerebral calcification
mental retardation
heart block
petechiae

HERPES SIMPLEX :
Pathophysiology :
Cutaneous portal entry of HSV from oral cavity/genital mucosa/ocular
conjunctiva/breaks in keratinized epithelia

Virus replicates locally , resulting in death of the cell & sometimes

produces clinically apparent inflammatory responses that facilitate the
development of herpetic vesicles and ulcers

Virus enters nerve endings & spreads beyond the portal of entry to
sensory ganglia by intraneuronal transport

Virus replicate in some sensory neurons

Progeny virions are sent via intraneuronal transport mechanism back to

the periphery , where they are release from nerve endings

And replicates further in skin or mucosal surfaces

Viral moving through this neural arc that is primarily responsible for the
development of characteristic herpetic lesions

*some infected neurons do not initially support viral replication , in this

neurons that the virus establishes a latent infection

a condition where :
viral genome persists within the neuronal nucleus in a largely
metabolically inactive state

reactivation of the latent neuron ,

progeny virions are produced

transported within nerve fibers back to cutaneous site somewhere in the

vicinity of the initial infection

further replication occurs

causes recurrent infections >>> asymptomatic

virus is shed at the site where cutaneous replication occurs

and can be transmitted to susceptible individual who came in contact with

contaminated secretions

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INFECTIOUS DISEASES

viremia/hematogenously spread of the virus

give rise to dissemination of the virus to visceral organs including liver

and adrenals and only in neonates into the brain

infections from maternal are transmitted to fetus generally occur during

delivery

most portal of entry are conjunctiva , mucosal epithelium of nose and

mouth and breaks or abrasions in skin due to scalp electrode use or
forceps delivery

if virus extend from :

- nose to respiratory tract >>> pneumonia
- move via intraneuronal transport to CNS >>> encephalitis
- spread by hematogenous dissemination to visceral organ and brain >>>
encephalitis

factors influenced neonatal HSV infections are :

- virus type
- portal of entry
- inoculum of virus to which the infant is exposed
- gestational age of infant
- presence of maternally derived antibodies specific to the
virus causing infections

Clinical manifestation :
1. Primary infection
Fetal loss
Congenital Syndrome
2. Recurrent
Mucocutaneous lesions
Disseminated disease
Encephalitis