Clinical Parasitology

Dr. Mohieddīn Abdul-Fattah

Introduction -Definitions• Parasitism :(التطفل) a relationship in which one organism

(parasite) lives at the expense of another (host).

• Endoparasite :( داخلى a parasite which lives within the (طفيلbody of the host, e.g. protozoa and helminthes

• Ectoparasite :( خارجى lives on the body surface of the (طفيلhost e.g. insects

• Habitat:( العائل داخل الطفيل the organ in which the (مقرparasite exists in the body of the host.

• Final host:( النهائى harbors the adult or sexually mature(العائلparasite.

• Intermediate host : ( الوسيط harbors the immature stages (العائلor asexual stages of a parasite that show significant development.

Definitions• Reservoir host : ( المخزن the animal that holds the (العائل

same stage of the same species of a parasite that man holds and contributes to the perpetuation of the parasite life cycle in nature.

• Transport host (Paratenic): the intermediate host that carries the larva of the parasite without significant development (with arrested development).

• Vector مخزن غير موجه an arthropod or a snail IH that ( :(ناقلdirects a parasite to a certain host within certain conditions.

• Exit stage ( الخروج The stage that gets out of the host :(طورand aids in diagnosis (diagnostic stage).

• Inlet stage or infective stage ( المعدى الطور أو االدخول :(طورThe stage that enters the host and causes the infection.

• Auto-infection ( الذاتية when a host infects himself; this :(العدوىoccurs when the infective stage is the exit stage.

• Patent infection: infection with an exit stage out of the host in clinical sample and which contributes to perpetuation of the life cycle.

• Non patent infection: infection without exit stage out of the host. • Routes of infection or entry of the infective stages:1. By ingestion of: larva, egg, cyst or oocyst in contaminated foods & drinks.2. Entry of larva, trophozoites, sporozoites or cysts through contact with skin ulcer

and abrasion, or by active penetration, or via inoculation by an insect.3. Through epithelia of mucosal surfaces, of the eye, olfactory epithelium or

respiratory tracts.4. Congenital transmission.5. Blood transfusion.

Host-Parasite Relationship1. Infection: means establishment of a parasite existence within

the host accompanied or not with its development and reproduction.

This means host parasite interaction passes through 4 stages: initial contact (contamination), establishment within suitable habitat, development and lastly reproduction.

2. Immune response:• When a parasite antigens come into contact with the host

immune system (cells), these cells interact with the parasite antigens (structures or excretion and secretions) to induce:

A. Parasite immune-evasion,

B. Host immune-protection (immunity or resistance)

C. Host immune-pathogenesis

D. or aid in immune-diagnosis.

Host-Parasite Relationship3. Disease (Pathogenesis):• The occurrence of infection does not necessarily

imply the occurrence of disease. • Disease only occurs if the anatomical and/or the

physiological integrity of the host were broken down. • If infection leads to this breakdown it induces disease.

Disease is usually presented by signs and symptoms.• Opportunistic infection: infection that does not

cause disease in immune competent host, but if the host immunity is impaired it does.

Host-Parasite Relationship

• How do Parasites damage their hosts?

1.Competing for nutrients (e.g. Hookworms and D. latum).

2.Disrupting tissues (e.g. Hydatid disease, myiasis and Tungiasis).

3.Destroying cells (e.g. malaria, hookworm, and schistosomiasis).

4.Mechanical blockage (e.g. Ascaris).

5.Severe disease often is induced by immune / inflammatory response.

Trematoda

Dr. Mohieddīn Abdul-Fattah

Trematodes According to Habitat

• Intestinal Trematodes:

1. Heterophyes

2. Metagonimus

3. Fasciolopsis

4. Echinostoma• Liver trematodes:

1. Fasciola.

2. Clonorchis

3. Opistorchis

• Lung trematodes:

1. Paragonimus.• Blood trematodes:

1. Schistosoma

Heterophyes heterophyes

• Final host: Man, dogs and cats

• Habitat : between villi in small intestine

• Exit stage: mature egg in stool of FH.

• Morphology: 1.5 x 0.5 mm, pear like trematode.

I. Biology

II. Epidemiology• Geographical distribution: Egypt around Borollos and

Menzella lakes , Palestine Europe and Far East..• Transmission:

1. Intermediate host (I.H.): Pirenella conica is 1st I.H. and Bolty and Boory fish are 2nd I.H.

2. Reservoir hosts: dogs and cats act as final reservoir hosts.

3. Infective stage: Encysted metacercaia in fish muscles

4. Mode of infection: Ingestion of insufficiently cooked or under salted fish infected with Encysted metacercaria

Host parasite relationship 1. Mild infection is almost asymptomatic

2. Heavy infection induces local intestinal inflammation and intermittent diarrhea

3. The small eggs may be inoculated into the blood vesels and migrate to heart and brain resulting in embolic manifestations.

4. Myocarditis and neurological complications are reported

IV. Diagnosis

• Detection of eggs in stool.

• Egg charcteristics:

1.30 x 15 µm,

2.oval, thick shelled,

3.yellowish brown, operculated

4.mature (contains developed larva [miracidium]).

V. Treatment

• Praziquantel; 25 mg/kg/8h PO for one day

VI. Control • Adequate salting and cooking of fish and

snail control.

• Proper disposal of human waste and eradication of stray dogs.

• Mass examination and treatment of fishermen and health education

Fasciola hepatica and F. giganticaI. BIOLOGY• Man, sheep and cattle act as final hosts. • Diagnostic morphology: A. 3-6 x1.2 cm, leaf like hermaphrodite B. with anterior conical part and posterior

elongated part C. having parallel lateral borders in F. gigantica

or converging in F. hepatica.• Habitat in the final host: The biliary tracts

of the liver. • Exit stage: Immature egg.

Lymnaea snail

Fasciola egg

Fasciola hepatica

Simple tailed cercaria

E. metacercaria on

grass

II. Epidemiology• Geographical distribution: Egypt and

sheep and cattle raising countries.• Transmission: 1. Intermediate host (I.H.): Lymnaea is

1st I.H. and vegetable is 2nd I.H.2. Reservoir hosts: Sheep and cattle act

as final reservoir hosts3. Infective stage: Encysted metacercaia4. Mode of infection: Ingestion of raw

vegetable contaminated with encysted metacercaia

III. Host-Parasite Relationship• Immune responses:Humoral: Early development of IgM, IgE, IgG1 and IgG2 to

ES Fasciola Ags. These are of limited role in protection.Cellular: Peripheral eosinophilia and lymphocytosis. The response in the invasive phase is due to Th1

cytokines.Th2 type cytokines predominate when the worms reside in

the bile canaliculi. • Effector protective mechanisms against JF : The toxic NO produced by IFNγ activated macrophages. ADCC; IgG1, IgE, IgA, IgG2a dependent macrophage,

eosinophil, and platelet cytotoxicity This leads to release of the killing granules: ECP, MBP and

eosinophil peroxides.

III. Host-Parasite Relationship• Pathogenesis:• Acute fasciolitic hepatitis during the migratory phase in

liver. It is manifestecd by fever, eosinophilia and allergic features.

• Chronic biliary fascioliasis when the worm resides in the biliary passages causing duct hyperplasia due to excessive proline secretion and biliary obstruction

• This→ jaundice and haematobilia → anaemia. The worm secreted proline also contributes to anaemia via its inhibitory effect on erythropioesis.

• Fasciolitic pharyngitis (Halzoun) caused by the presence of adult in the pharynx after eating infected raw sheep liver infectd with adults..

Pathogenesis

The surface spines of Fasciola damage the biliary epithelium during chronic stage

Juvenile Fasciola migrating in liver parenchyma during invasive stage

IV. Diagnosis• Detection of eggs in stool.

Direct and conc.• Egg charcteristics: 1. thin walled, 2. 140 x 70 µm, 3. ovoid, 4. yellowish brown,

Operculated, 5. immature (does not contain

developed larva [miracidium]).

Indirect diagnosis

Serodiagnosis (sp. during invasive stage)

• IFAT (T.S of adult worm) or ELISA (ES ags).

Imaging: CT sonography

V. Treatment• Triclabendazole (10 mg/kg PO for one dose)

or Mirazid.

VI. Control1. Adequate washing of vegetable.

2. Mass treatment of Reservoirs.

3. Sanitations of slaughter houses.

4. Control of snails.

5. Proper disposal of human waste.

Paragonimus westermani

Final host: Humans, dogs, cats, rodents and pigs.

Habitat: Encapsulated in the bronchioles of the lung

Exit stage: immature eggs passed in feces and sputum. Basic morphology and life

cycle: adult thick bodied 4 mm x 8 mm.

I. Biology

Adult

Egg in sputum

II. Epidemiology Distribution: worldwide but more confined

in oriental countries such as Japan. Reservoir hosts: Dogs, cats, rodents and

pigs. Intermediate hosts: 1st IH snail;

Semisulcospira or Thiara and 2nd fresh water cructaceans.

Infective stage: Encysted metacercaria in gills and muscles of crustaceans (crabs).

Mode of infection: ingestion of encysted metacercaria in undercooked crustacean.

III. Host Parasite Relationship Early symptoms cough with blood tinged sputum.Low grade fever Difficult

to distinguish from pneumonia and

tuberculosis.Ectopic sites may

include: abdominal wall, heart, lymph nodes and

nervous system.

T.S. of lung containing encapsulated adult

Eggs in m. LN with granulomas abundant with esosinophils

IV. Diagnosis

Clinical picture with eosinophila in endemic

areas.Detection of eggs in

sputum or feces.Serology for ectopic

sites DIG or ELISA.Imaging: plain x-ray.

V.Treatment

• Praziquantel; 25mg/kg/8h PO for 2 days

• Bithionol ; 20 mg/kg/12h Po daily for 14 ds.

VI.Control• Health education.

• proper cooking of crabs and crayfish .

Schistosoma mansoni & S. hematobium• BIOLOGY Man only acts as final hosts.

Diagnostic morphology: sex separate flukes.

Male is ~ 20 mm covered with tubercle, flattened dorso-ventrally and folded on it self to form gynecophoric canal.

Female is ~ 26 mm cylindrical and smooth carried by the male. Habitat in the final host:

Inf. mesenteric veins draininnig large intestines in S. mansoni. vesical plexus draining urinary bladder in S. hematobium.

Exit stage: mature egg in stool (S.mansoni) and in urine (S. hematobium).

II. Epidemiology Geographical distribution: Africa, south America,

Middle East and Portugal. Transmission:

1. Intermediate host (I.H.): The snails; Biomphalaria is I.H. of S.mansoni and Bulinus is I.H. of S

hematobium.

2. Reservoir hosts: No animal reservoir hosts.

3. Infective stage: Free swimming cecaria in fresh water

4. Mode of infection: free cercaria penetrates skin

III. Host-Parasite Relationship

A. Early cell mediated immunity before egg laying.

B. Late humoral antibody dependent cell mediated cytotoxicity (ADCC).

• Immune responses:

• Pathogenesis1. Cercarial dermatitis (swimmer's itch): maculo-papilar rash in areas of skin exposed to cercaria S.

haematobium, S.mansoni and to avian schistosome infection.

– It is due to immediate or late hypersensitivity reaction that begins 1-2 days after exposure. It

more common among the newcomers to endemic areas.

2. Acute schistosomiasis (Takayama fever): fever occurs weeks after the primary infection.

– It is due to massive IFN-γ and TNF-α cytokines of TH1 response priming for granuloma formation

around the eggs.

• Pathogenesis1. Chronic schistosomiasis: occurs due to TH2

cytokine response that strongly expands the granuloma size.

2. The cellular components of this granuloma are plenty of eosinophils plus macropages,

fibroblasts and lymphocytes. Eosinophil mediated chronic inflammatory reactions predispose to

fibrosis around the eggs in tissues of the affected organs.

3. Downregultion of fibrosis is associated with diminshed TH2 cytokines and increased TH1

cytokines.

Pathogenesis

Cercarial dermatitis

Adult in lung

Planorbis

granulomas in lung Egg granuloma in liver

• Pathogenesis• The manifestations in the chronic stage include:

In S. mansoni:a) Colonic polyps with bloody diarrhea

b) Periportal fibrosis → portal hypertension with hematemesis and splenomegaly.

In S. hematobium:a) Cystitis (sq cell carcinoma), ureteritis with hematuria.

b) Ureteric stricture induces hydronephrosis

c) CNS disorders and core pulmonale occur earlier in S.hematobium due to direct passages of eggs from

bladder and ureteral veins into systemic veins than in S. japonicum and mansoni.

d) In the latters they occur later after the onset of portosystemic shunts.

Portosystemic shunts1. esophageal varices;

2. paraesophageal varices;

3. gastrorenal shunt; 4. splenorenal shunt; 5. inferior

mesenteric, hemorrhoidal, & internal iliac veins

6. mesocaval shunt; 7. intrahepatic

portosystemic shunt;

8. Sappey's veins

Pathogenesis

Colonic polyps endoscopy

Polyposis post mortem

Eggs in C. polyp biopsy

B splenomegalyPeriportal fibrosis

Periportal fibrosis

Esophageal varices

Pathogenesis (hematobium)

Ureteral dilatation due to calcified stenosis of orifices

Rt unilateral hydronephrosis

Squamous cell carcinoma of bladder. Ova of hematobium are often found in such tumour

Fetal head appearnce due to intense calcification of bladder→

IV. Diagnosis Detection of eggs in stool (S.mansoni) or in urine

(S.hematobium).

Egg characteristics:

o S. mansoni: Ovoid non-operculated, 140 x 70 µm, yellowish brown with lateral spine and mature (contains

miracidium).

o S. hematobium: spindle shaped, non-operculated, 140 x 70 µm, yellowish brown with terminal spine and mature

(contains miracidium).

o Serology in prepatent and chronic infection to detect specific schistosome antigens and antibodies

V. Treatment• Praziquantel; 40 mg/kg PO with food divided

into 2 doses separated by 4-6 hours for S. mansoni and hematobium .

VI. Control

1. Avoiding swimming in fresh water.

2. Proper disposal of human waste.

3. Control of snails and health education.

4. Mass treatment