There are nearly 100 viruses of the herpes group that infect many different animal species. Official name of herpesviruses that commonly infect human is Humans herpesvirus (HHV) herpes simplex virus types 1 (HHV 1) Herpes simplex virus type 2 (HHV 2) Varicella-zoster virus (HHV 3) Epstein-Barr virus, (HHV 4) Cytomegalovirus (HHV 5) Human herpesvirus 6 (HHV 6) Human herpesvirus 7 (HHV 7) Human herpesvirus 8 (HHV 8) (Kaposi's sarcoma-associated herpesvirus). Herpes B virus of monkeys can also infect humans hELMINTHS#corona virus#Aspergillosis#BUGANDO#CUHAS#CUHAS#CUHAS

1. TOXOPLASMOSIS
DR.HAMISI MKINDI,MD.
TO DOWNLOAD CONTACT: hermyc@live.com

2. OVERVIEW
Toxoplasmosis is caused by infection with the
protozoan Toxoplasma gondii, an obligate
intracellular parasite.
Certain individuals, are at high risk of severe or life-
threatening disease due to this parasite.
These include congenitally infected fetuses, newborns
and immunologically impaired individuals
Congenital toxoplasmosis is the result of maternal
infection acquired during gestation.

3. In immunodeficient patients,toxoplasmosis
most often occurs in persons with defects
in T cell–mediated immunity such as those
receiving corticosteroids, anti–tumor
necrosis factor (TNF) therapies, or
cytotoxic drugs and those with malignance,
organ transplants, or acquired
immunodeficiency syndrome (AIDS).

4. In immunocompetent individuals, primary
or chronic (latent) infection with T. gondii is
asymptomatic; after the acute infection, a
small percentage has chorioretinitis,
lymphadenitis, or, even more rarely,
myocarditis and polymyositis
In 1983, the first report of toxoplasmosis in
AIDS patients appeared.Toxoplasmic
encephalitis (TE) subsequently was
recognized as the major cause of space-
occupying lesions in the brains

5. ETIOLOGY AND LIFE CYCLE
T. gondii is a coccidian parasite of felids
with humans and other warm blooded
animals serving as intermediate hosts.
It belongs to the subphylum Apicomplexa,
class Sporozoa
Its infectious frorms includes the oocyst,
the tachyzoites(group or claster of oocyst)
and tissue cyst (which contains and may
release bradyzoites),

6. Most organisms isolated from both
animals and humans can be grouped into
one of three clonal genotypes (types I to III)
Type III strains are common in animals but
observed significantly less often in cases
of human toxoplasmosis; most cases in
humans are caused by type II strains.
Both type I and II strains have been
associated with human congenital toxopl

7. 1. OOCYST
Cats sheds oocysts after they ingest any
of the three forms of the parasite, at which
time an enteroepithelial cycle begins.
 This sexual form of reproduction begins
when the parasites penetrate the epithelial
cells of the small intestine and initiate
development of asexual and sexual
(gametogony) forms of the parasite.
Oocyst wall, oocysts are discharged into
the intestinal lumen by rupture of intestinal
epithelial cells.

8. 2. TACHYZOITE
Tachyzoites are seen in both primary and
reactivated infection; their presence is the
hallmark of active infection.
Once the tachyzoite has invaded the
target cell, it can undergo stage
conversion into the bradyzoite form.

9. 3. TISSUE CYST
Tachyzoites multiply rapidly and
synchronously, forming more slowly
replicating bradyzoites which forms tissue
cysts.

10. VIRULENCE FACTORS
Its anterior end consist Conoid assist
parasites entrace into host cells
Rhoptries which has secretory functions
for parasitic invasion.
It has Dense granules in its cytoplasm
which release parasitophorous
vacuole,which also assist its entry.

14. The oocysts survive better in
environments with hot,humid climate
and lower altitude. Infection rate is
often highest in this area.
EPIDEMIOLOGY

17.  T.gondii can favor mother to child transmission HCV,HBV and HIV
verticle transimmision.
 According to this study,336 pregnant women were enrolled for
investigation on the presence of serum antibodies agaist
T.gondii,HCV,HBV and HIV using ELISA, the prevlance of
T.gondii,HCV and HBV was 25.3%,5.4%,9.8% respectively
 HIV serostatus 61.6 % seems to be associated with greater
prevalance rate of both T. gondii 28.5% vs 20.2% and HBV 11.6%
vs 7%.

18.  Untreated T.gondii infection are often fatal in AIDS patients, IgG
agglutination and PCR was used to analyse blood samples from
130 HIV positive patient in Uganda.
 Anti T.gondii were detected in 54% of the patient,while 23% had
parasites in the paripheral blood.

19.  This study reveals 30.9% of 350 pregnant women were
seropositive for toxoplasma gondii specific antibodies

21. The Study done by Elichilla Shao et al
‘sero-prevalence and factors associated
with Toxoplasma gondii infection among
pregnant women antending ANC at KCMC
in 2015 revealed 60 of 144(41.7%)
pregnant women were seropostive for
T.gondii specific Abs

22. PATHOGENESIS
Attachment to the host cell membrane
requires the calcium-dependent secretion of
adhesins.
T. gondii multiplies intracellularly at the site
of invasion (the gastrointestinal tract is the
major route for and the initial site of
infection in nature)
Invasion is an active process relying on
parasite motility and the sequential
secretion of proteins from secretory

23. Organisms may spread first to the
mesenteric lymph nodes and then to
distant organs by invasion of lymphatics
and blood
Tissue cyst formation takes place in
multiple organs and tissues during the first
week of infection, which are responsible
for chronic or residual or latent infection
and persists primarily in the brain, skeletal
and heart muscle, and eye.

24. In immunocompetent individuals, the initial
infection and the resultant seeding of
different organs lead to a chronic or latent
infection without clinical significance
Toxoplasmosis in immunodeficient
individuals may be caused by primary
infection
It most often is the result of reactivation of
a latent infection.

25. It is widely held that reactivation is the
result of disruption of the tissue cyst form
followed by uncontrolled proliferation of
organisms and tissue destruction.
After invasion, the humoral and cellular
immunity become activated
 Only those parasites protected by an
intracellular habitat or within tissue cysts
survive.

26.  An effective immune response reduces
the number of tachyzoites in all tissues.
Tachyzoites are killed by reactive oxygen
intermediates,acidification,osmotic
fluctuations and reactive nitrogen
intermediates and specific antibody
combined with complement

27. PATHOLOGY 1/3
CENTRAL NERVOUS SYSTEM
•Damage to the CNS
o Multiple foci of enlarging necrosis and microglial
nodules.
o Periaqueductal and periventricular vasculitis with
necrosis
•Hydrocephalus
o Obstruction of the aqueduct of Sylvius or foramen
of Monro.
•Multiple brain abscesses
• Severely immunodeficient

28. EYE
•Chorioretinitis in AIDS patients is characterized by segmental
panophthalmitis and areas of coagulative necrosis associated with
tissue cysts and tachyzoites
LUNGS
•Interstitial pneumonitis, necrotizing pneumonitis, consolidation,
pleural effusion, empyema, or all of these.
SKELETALAND HEART MUSCLES
•Myositis & Myocarditis has been reported in some HIV-infected
patients who present with neuromuscular symptoms
LYMPH NODES
•Frequently distinctive and often diagnostic, a reactive follicular
hyperplasia is seen always
PATHOLOGY 2/3

29. CLINICAL FEATURES 1/2
Imunocompetent patients
• Only 10% to 20% of cases of T. gondii infection in adults
and children are symptomatic, benign and self-limited
(Symptoms, if present, usually resolve within a few
months)
• Cervical lymphadenopathy discrete and nontender, are
rarely greater than 3 cm in diameter, may vary in
firmness, and do not suppurate.The nodes may be tender
or matted.
• Fever, malaise, night sweats, myalgias, sore throat,
maculopapular rash, hepatosplenomegaly, and small
numbers of atypical lymphocytes (<10%) may be present.

30. Immunocompromised Patients
• In HIV-infected patients, the incidence of toxoplasmosis is
closely related to CD4 T cell counts, with an increasing risk
when the count falls under 100 cells/l.
• Toxoplasmic encephalitis (TE):
o Most predominant manifestation, symptoms ranging from
headache,lethargy, incoordination, or ataxia to hemiparesis, loss of
memory, dementia, or focal to major motor seizures, usually associated
with fever
• Other organs: lungs, the eyes, and the heart, but the isolation
of Toxoplasma from many other sites, such as liver, pancreas,
bone marrow, bladder, lymph nodes, kidney, spleen, and skin
has been documented
CLINICAL FEATURES 2/2

31. • Classically, Primary acquired maternal infection during
gestation.
• Risk
• Less than 10%, 30%, 60-70% of cases during the first
trimester, 2nd and 3rd Trimester respectively
• Major sequelae:
o Mental retardation, seizures, microcephalus ,
hydrocephalus, deafness, and psychomotor deficiency.
o Eye: Microphthalmia, cataract, increased intraocular
pressure, strabismus, optic neuritis, and retinal necrosis,
uveitis and retinochoroiditis can be observed
• Characteristic triad: Chorioretinitis, Hydrocephalus and
Cerebral calcification
Congenital toxoplasmosis

32. DIAGNOSIS

33. Isolation
• Mouse inoculation or inoculation in tissue
cell cultures
• Isolation of T. gondii from blood or body
fluids establishes that the infection is acute

34. Histio & Cytopathology
Cytology
Eg CSF, BAL, Amniotic fluid
• Tachyzoites may be identified
Tissue biopsy (H&E) - Difficult
immunohistiochemistry- better
• Multiple tissue cysts near an inflammatory
necrotic lesion

35. Imaging Studies
CT scanning in cerebral toxoplasmosis
(general)
•Multiple bilateral cerebral lesions but may be
solitary.
MRI has superior sensitivity
Ultrasonography
•Ultrasonographic diagnosis of congenital
toxoplasmosis in a fetus is available at 20-24
weeks' gestation.

36. Ct scan images
Unilateral lesion Symmetrical lesion

37. Treatment 1/3
Acute infection
•Sulphadiazine tabs 1 gm 6 hourly +
Pyrimethamine tabs 100mg loading dose, then
50mg /day + Folic acid tabs 10mg /day for 6
weeks.
•Clindamycin capsules 450mg -600mg 6 hourly
+ Pyrimethamine tabs 100mg loading dose, then
50mg /day for 6 weeks.
Source: Tanzania, National guidelines for the management of HIV and AIDS

38. Treatment 2/3
After six weeks of treatment
• Give prophylaxis therapy with Sulphadiazine
tabs 500mg 6 hourly + Pyrimethamine tabs 25-
50mg /day + Folic acid tabs 10mg /day.
For those allergic to sulphur replace
Sulphadiazine tabs with Clindamycin capsules
450mg 6 hourly
• Discontinue maintenance therapy when CD4
count is >200cells/ml, initial therapy is
completed and patient is asymptomatic.
Source: Tanzania, National guidelines for the management of HIV and AIDS

39. • Primary prophylaxis therapy for toxoplasmosis
can be accomplished with Trimethoprim–
Sulphamethoxazole (TMP-SMX) tabs
160/800mg administered orally/day.
• For those allergic to sulphur, give Dapsone
tabs 50mg/day + Pyrimethamine tabs 50mg per
week + Folic Acid tabs 10mg 3 times a week
Treatment 3/3

40. Primary Prevention

41. • Treatment of pregnant women to reduce parasite
transmission.
• Screening
o Prenatal screening and treatment to limit fetal damage.
o Postnatal screening of neonates to promote early
treatment.
o Screening Immunocompromised Patients
• Prophylaxis of TE in Toxoplasma-seropositive AIDS
patients is rather consensual, and Cotrimoxazole
prophylaxis should be administered when the CD4 T cell
count falls below 100 cells/l. since it is also suited
for(PCP) prophylaxis.
Secondary Prevention

42. REFERENCES
• Mandell,Bennett &Dolin,Principels and Practice of Infectious Diseases 6th
edition
• Epidemiology of and Diagnostic Strategies for Toxoplasmosis-Florence
Robert-Gangneuxa,b and Marie-Laure Dardéc 2012
• Sero-prevalence and factors associated with Toxoplasma gondii infection
among pregnant women attending antenatal care in Mwanza, Tanzania-
Mwambe et al. Parasites & Vectors 2013, 6:222
• High seroprevalence of specific Toxoplasma gondii IgG antibodies among
HIV/AIDS patients with immunological failure attending a tertiary hospital
in northwestern Tanzania-Mirambo et al 2013
• Sero-Prevalence and Factors Associated with Toxoplasma Gondii Infection
among Pregnant Women Attending Antenatal Care in the Referral Hospital
in Tanzania: Cross Sectional Study-Shao et al 2014
• Tanzania, National guidelines for the management of HIV and AIDS, 7th
Edition, 2019