Plasmodium Schistosoma Cryptosporidium Taenia

Malaria
Hosts Definitive: Man Definitive: Man Man (sexual and asexual Definitive: Man
Intermediate: Anophales Intermediate: Fresh water snails cycle occurs in single host) Intermediate:
Mosquito T. Solium: Pig
T. Saginata: Cow
Infective Stage Sporozoite stage Fork-tailed cercaria Sporulated oocyst in food Cysticercus bovis - T. saginata
and water Cysticercus cellulosae - T. solium
Diagnostic Gametocyte stage Eggs in urine or stool Oocyst in stool Eggs in stool
Stage
Mode of Mosquito bite/ in some Cercaria penetrating the skin of • Ingestion of thick walled T. Solium: undercooked pork
Transmission types blood transfusion host oocysts containing cysticercus cellulosae
• Contaminated food or ingestion of egg in contaminated
or drink food, water, etc
Heteroinfection T. Saginata: undercooked beef
• Faeco-oral route containing cysticercus bovis
External
autoinfection Cysticercosis:
• Thin-walled oocysts External autoinfection - faeco-
intestine of already orally
infected patient Heteroinfection: ingestion of T.
Internal solium eggs
autoinfection Internal autoinfection: adult T.
soliumworms lay eggs causing
cysticercosis
Pathogenesis 1. Liver phase • Cercaria penetrate the skin • Intestinal villi show: • Scolex anchors to the intestine and
• Mosquito injects • Schistosoma finds its way into • Inflammatory causes an inflammatory reaction
sporozoite venous circulation and settles changes causing
• Sporozoite goes in the liver atrophy/ crypt
to liver when it is • Adult shistosoma resides in the hyperplasia
either active (All big vein while the females more • In immunocompromised
species) or through the venules to lay eggs patients:
 becomes dormant • Eggs enter the veins or • Dissemination of
(vivax and ovale) continue circulation cryptosporidium
• Parasite divides to parvum occurs to:
make shizont Stages: esophagus, gall
• Cell ruptures, • Stage 1 - invasion bladder, respiratory
releasing • Stage 2 - migration tract, urinary
merozoites • Stage 3 - egg deposition bladder
Patient is asymptomatic and extrusion Cryptosporidium parvum
2. Blood phase • Stage 4 - tissue reaction are opportunistic
• Liver merozoite
enters RBC -> ring
stage
• Trophozoite stage
that then turns
into a schizont
• RBC ruptures
• Blood merozoites
continue
development and
enter gametocyte
stage
Patient is symptomatic
Clinical Picture *Symptoms coincide • During stage 1 (1-4 days) • In immunocompetent • Intestinal disturbances
with rupture of infected • Local dermatitis, subject: • Intestinal obstruction
RBCs, release of irritation, papular rash • Mild, self-limited • Loss of weight
parasite metabolites • During stage 2 (3-4 weeks) diarrhea for 2 weeks • Neurological manifestations
and host immunological • Metabolic products cause • Children • Acute appendicitis
response toxic and allergic • Abdominal • Cholangitis
1. Patient passes into 3 manifestations like discomfort, diarrhea, • In T. solium only:
stages: urticaria, fever, headache, anorexia • Cysticercosis
1. Cold stage muscle pain • Immunocompromised
2. Hot stage • Lung - pneumonitis, patient
3. Sweating stage hemoptysis • Severe life-
2. Hemolytic anemia • Liver - enlarged and threatening
tender diarrhea,
 3. Enlargement of spleen • During stage 3 (1-2 months, dehydration and
and liver acute) malabsorption
4. Attacks dec until the • Female releases egg
disappear but reappear antigen causing fever,
when: rigors, abdominal pain
1. Hypnozoites • Katamaya syndrome:
cause a relapse mainly in S. japonicum
2. Recrudescence o Fevers, chills,
diarrhea,
generalized
lymphandenopathy
• During stage 4 (months/years,
chronic)
• Bladder - bladder cancer
when egg becomes
trapped
• Kidney - hydroureter and
hydronephrosis
• Colon - polyps in S.
mansoni infection
• Embolic lesions in both S.
hematobium and S.
mansoni if eggs fail to fix
to venule wall
o Embolic lesions in
patients liver
o Ascites and
hepatosplenomegaly
o Embolic lesions in
patients lung
o Congestive heart
failure
Diagnosis • Thick and thin blood film • Clinically • Watery diarrhea • Detection of eggs and/or gravid
• History of contact with • Stool analysis segments in stool
infected water • Direct smear • Stain eggs with ziehl neelsen stain:
 • Detect circulating • Laboratory
parasite antigen using
monoclonal antibodies
Treatment Drug Resistant - Artiminisin Praziquantel
Tissue Shizonticides:
Primaquine/pyrimethamine
Blood Schizonticides:
Chloroquine/Mefloquine
Blood gametocytes:
Chloroquine/primaquine
Additional Plasmodium Malariae Shistosoma mansoni:
Information Complication:
• Nephrotic
Syndrome
Plasmodium Falciparum
Complication:
• Knob formation
• Hyper-reactive
splenomegaly
• Concentration • If they stain -> T. saginata
• Direct methods (detection method • If they don't stain -> T. solium
of Schistosoma Modified Ziehl-
hematobium egg in urine Neelsen stain or Diagnosis of Cysticercosis:
or detection of immunofluorescence • Blood examination - increase
Schistosoma mansoni assay must be used eosinophils
eggs in stool) • Detection of antigen in • Serological tests - anti-taenia
• Serological tests (anti- stool antibodies or antigens
schistosoma antibodies) • Intestinal biopsy • X-ray, MRI, CT
• Blood examination
(anemia, hypersplenism)
• Radiological imaging
o S. hematobium -
calcified bladder
with hydroureter
and hydronephrosis
• Endoscopy
• Immunocompetent: self- Praziquantel
limited Saline purge after T. solium infection
• Immunocompromised:
Nitazozanide & fluid and Treatment of Cysticercosis:
electrolyte replacement • Praziquantel
• Surgical treatment
• Steroids
• Vitamin D and calcium
• Parasite lives in inferior
mesenteric plexus of veins
• Egg in stool
• Intermediate host: B.
alexandrina snail
• Eggs of lateral spine
 • Black water fever Schistosoma hematobium:
Resistance: • Parasite lives in vesical and
• Absence of duffy pelvic plexus of veins
antigen - resistant • Egg in urine
to P. vivax • Intermediate host: B.
• Hemoglobin S - truncatus snail
resistance to P. • Eggs have terminal spin
falciparum Schistosoma japonicum:
• Deficiency of CP6D • Parasite lives in superior and
- resistance to P. inferior mesenteric plexus of
falciparum veins
• Plasmodium vivax
o Benign tertian
malaria
o Relatively benign
o Develops
Hypnozoites
o Rupture of RBC
happens every 3rd
day
o Invades young RBCs
o Malaria pigment
called schuffner's
dots
• Plasmodium ovale
o Ovale tertian
malaria
o Relatively benign
o Develops
Hypnozoites
o Rupture of RBC
happens every 3rd
day
o Invades young RBCs
o Malaria pigment
called schuffner's
dots
• Plasmodium malariae
o Quartan malaria
o Relatively benign
o Rupture of RBC
happens every 4th
day
o Leads to nephrotic
syndrome
o Invades old RBCs
o Malaria pigment
called Ziemann's
dots
• Plasmodium falciparum
o Malignant tertian
malaria
o Rupture of RBC
happens irregularly
o Invades RBCs of any
age
o Leads to knob
formation on the
surface of infected
RBCs, hyper-reactive
malarial
splenomegaly and
black water fever
o Malaria pigment is
called maurer's cleft
 Enterobius
Vermicularis
Hosts No intermediate host
Entire cycle in human
Infective Stage Egg containing larva
Diagnostic Stage Detection of eggs
Mode of Ingestion of Enterobius eggs:
Transmission • In contaminated food or
drink
• Autoinfection (hand to
mouth)
Pathogenesis • Ingested egg in
contaminated food, drink
,etc
• Eggs hatch and larva pass
through intestinal lumen
• Larvae then matures to
become an adult
• Females migrate during the
night and lay eggs
Clinical Picture • Pruritus ani
• If female worms migrate to
abnormal site:
• Urethra
o Urinary infection
Cutaneous Leishmaniasis
Definitive: Man
Intermediate: Sand fly
Promastigote
Amastigote
Bite of an infected female sand fly
Vertical transmission from mother to fetus, Vertical transmission from mother to fetus, blood
blood transfusion
1. Promastigotes are engulfed by skin
macrophage
2. Promastigote -> amastigote and it
multiplies in the skin macrophage until 3. Amastigotes are then taken up by reticulo-
it ruptures
3. Inflammatory cells are attracted to the
site
4. Nodule forms at the site of the bite due
to multiplication of leishmania in the
skin
5. An ulcer forms with a sharp-cut
indurated margin and over the course
of a year the healing occurs ->
disfiguring scar
Visceral Leishmaniasis
Definitive: Man
Intermediate: Sand fly
Promastigote
Amastigote
Bite of an infected female sand fly
transfusion
1. Skin macrophages also engulf the promastigotes
2. Promastigotes -> amastigotes and causes the
macrophage to burst
endothelial cells in the patient’s viscera
a. Liver -> hepatomegaly
b. Spleen -> splenomegaly
c. Lymph nodes -> enlarged
d. BM -> anemia
1. Fever
a. Intermittent with double daily rise – called
dum-dum fever
2. Hepatosplenomegaly
3. Skin changes
a. Disturbance of pigmentation
 o Involuntary b. Dark pigmentation (kala azar – butterfly
micturition pigmentation)
• Appendix 4. Post kala azar dermal leishmanoid (PKDL)
o Appendicitis a. Skin nodules
• Fallopian tube b. Persistent allergic reaction to parasite
o Vulva-vaginitis antigens
o Pelvic peritonitis c. Seen in:
• Intestinal diarrhea and i. Spontaneous arrest of the disease
abdominal pain ii. Incomplete antimony treatment
5. Weight loss, emanciation, death from inner-
current infection
a. Leishmanial causes suppression of cell-
mediated immunity of infected patient
b. Such as pulmonary infections, GIT, cancrum
oris
Diagnosis • Clinically: 1. Clinically 1. Detection of amastigotes in blood or tissue
• Pruritus ani at night a. Ulcer with sharp indurated margin a. In blood:
• Laboratory - perianal swab 2. Microscopy i. Amastigotes are typically low in # in the
to detect eggs a. Aspirate at the edge of the ulcer patient’s blood as they are taken by the
• NIH swab to detect amastigotes RES in spleen, liver, etc
• Scotch adhesive state 3. Culture ii. By thick drop preparation
a. Of aspirate or scraping from edge iii. Buffy coat method – concentration
of the ulcer on suitable medium technique where you centrifuge the
to detect promastigotes blood and take the buffy coat to analyze
b. After isolation, parasites can be under a score
characterized to the species level b. In tissue:
using isoenzyme analysis i. Take a biopsy from liver, spleen, lymph
4. Intra-dermal test (Montenegro test) node, none marrow and stain with
a. Using leishmanial antigen from giemsa stain
cultured promastigotes 2. Culture
b. Appear as indurated area after 3 a. Of patient’s blood or material from liver,
days spleen, lymph node or BM on suitable
medium to detect promastigotes
b. Isoenzyme analysis- characterizes species
3. Serological tests
 a. Detect anti-leishmania antibodies
4. Molecular techniques
a. PCR – DNA of parasite in blood or tissues
b. Advantage: rapid, results within days,
sensitive, identifies species
c. Disadvantage: expensive, highly equipped lap
Treatment Albendazole 1. Physical method: Antimony Sodium gluconate (Pentostam) – given
White mercury oxide a. Surgical excision – removing the intramuscularly
whole thing
b. Curettage (remove parts that are
on the outside – to clean it)
c. Heat, freezing
2. Chemical method
a. 2% chloropromazine &
clotrimazole
3. Interferon gamma
a. Injected intradermaly around the
lesion in order to promote healing
of the ulcer
Additional
Information