SCHISTOSOMES Flashcards

1
Q

Schistosomes Epidermiology

A

*Schistosomes are dioecious, (sexes are separate) trematodes.
*Causes Schistosomiasis (bilharziasis)
*Affects millions of persons in Africa, Asia, and Latin America

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

S. hematobium distribution

A

Africa and the Middle East

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

S. japonicum distribution

A

Endemic in the Far East, Southeast Asia and the Philippines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Epidemiological patterns of schistosomiasis

A

*High rates of infections are seen in farmers, fishermen & children.
*Infection is related to frequency of water contact measured as duration, frequency, and area skin surface.
*Presence of snail intermediate host.
*Environmental contamination resulting from indiscriminate human excreta disposal

*Levels of infection: Intensity measured as eggs/gram of stool or eggs/10ml urine.

*Number of eggs proportional to mated females

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Schistosoma mansoni infection and habitat

A

*Causative agent for Intestinal schistosomiasis

Habitat:
*Mesenteric vein predominantly in the inferior mesenteric vessels surrounding the large intestine.

*Also the intra hepatic portion of the portal vessel.

All schistosomes live in venous plexuses in the body of the definitive host, location varying with the species.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

GENERAL MORPHOLOGY OF SCHISTOSOMES

A

*Males:-6-12 mm long. 6-9 testes
=lateral margins of the male are rolled ventrally into a cylindrical shape producing a long groove or gynecophoric canal, in which the female is held.
=Integument tuberculate

*Females:-7-17 mm long & slender.
=Uterus is short and contains few eggs (1–3 eggs).
The adult worms are smaller & their integuments studded with prominent coarse tubercles

*Eggs has a lateral spine, partly mature when laid.
=The prepatent period (the interval btwn cercarial penetration & beginning of egg laying) is 4–5 weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Hosts and Infective form of schistosomes:

A

=Definitive host: Humans are the only natural definitive hosts.

=Intermediate host: Fresh-water snails of the genus Biomphalaria.

=Infective form: Fork-tailed cercaria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

LIFE CYCLE OF SCHISTOSOMES

A

①The schistosomulae mature in the liver & the adult worms move into the venules of the inferior mesentery
⓶Eggs laid in submucosa venules & mucosal layers, escape into the lumen of the intestine.
③Eggs in feces. Transparent shell, yellowish and have lateral spine.
④After deposition in the tissues, eggs shell enlarges and miracidium grows and develops.
⑤Eggs secrete enzymes that facilitates passage through tissue into lumen
=Eggs are mature when passed into feces
⑥On contact with fresh water, the eggs hatch to release miracidium
=Miracidium invade snail intremediate host – Biomphalaria sp
=1st and 2nd Generation sporocysts present
=Cercaria develop in the second generation (‘daughter’) sporocysts.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

PATHOGENESIS OF S. MANSONI (3 SUCCESSIVE STAGES)

A

①Skin penetration by cercariae.
⓶During maturation and at the beginning of oviposition.
③During the stage of egg deposition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Skin penetration by cercariae

A

A self-limiting pruritic rash called cercarial dermatitis or swimmers itch may develop locally. 24-36 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

During maturation and at the beginning of oviposition.

A

=Acute schistosomiasis or Katayama fever (a serum sickness-like syndrome) with fever, rash, myalgia, arthralgia, cough, generalized lymph adenopathy, and hepatosplenomegaly may develop.

=Individual with acute schistosomiasis show high peripheral blood eosinophilia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

During the stage of egg deposition.

A

=Symptoms mainly intestinal as the eggs are deposited in the small intestine.
=This condition is known as intestinal bilharziasis or schistosomal dysentery.
=Patients develop colicky abdominal pain and bloody diarrhea
=Eggs deposited in gut wall cause inflammatory reactions causing micro abscesses, granulomas & eventual fibrosis.
=Some of the eggs are carried through portal circulation into liver causing periportal fibrosis.
=Portal hypertension due to fibrosis may cause GIT hemorrhage
=Artriovenous shunts in intestine and periportal fibrosis lead to oesophageal varices which can bleed.
=Ectopic egg deposition can occur in the spinal cord, Kidneys, myocardium, lungs, pancreas, adrenals- corresponding pathologic symptoms
=Growth retardation by chronic infection with Schistosoma mansoni

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Egyptian splenomegaly:

A

The combination of enlarged, irregularly fibrosed liver, and greatly enlarged spleen is commonly called ‘Egyptian hepatosplenomealy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

DIAGNOSIS of Schistosoma mansoni

A

①As soon as egg extrusion begins characteristic lateral spined eggs are seen in stools.
Concentration method & Kato-Katz thick fecal smears are used.

⓶Serological Diagnosis by detecting schistomal antigen and antibody

③Rectal snips, scrapings, aspirates, biopsy via proctoscopy.
④Pulmonary complications ,X-ray imaging used, =Eggs in sputum sometimes.
⑤Imaging:- Ultrasonography (USG) is useful to detect hepatosplenomegaly and periportal fibrosis.
⑥Blood Examination may reveal eosinophilia & increased levels of alkaline phosphatase.
⑦Egg in urine samples - occasionally

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

TREATEMENT OF INTESTINAL SCHISTOSOMIASIS

A

①Praziquantel – drug of choice single dose 40mg/kg

⓶Oxaminiquine – Is also effective. It damages the tegument of the male worm making the worm more susceptible to lethal action of the immune system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Schistosoma haematobium Infection and Habitat

A

=Causes urinary bilharziasis

Habitat:
=The adult worms live in the vesical and pelvic plexuses of veins.
The adult worms may live for 20–30 years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Morphology of S. haematobium:

A

=Male: 10 – 15mm with minute tuberculations
gynecophorirc groove where female is held, 4 -5 testes.

=Female:20mm long & slender, extremities tuberculated.
*The gravid worm contains 20–30 eggs in its uterus at one time & may pass up to 300 eggs a day

=Eggs are ovoid with a terminal spine at one pole.
The terminal spine being characteristic of the species.
*Egg partly mature when laid

18
Q

Mechanism of Egg Expulsion in S. haematobium

A

=Eggs laid in small venules of the vesical & pelvic plexuses
=Sometimes in mesenteric portal system, pulmonary arterioles & other ectopic sites.
=Eggs pass into the bladder assisted by piercing action of spine & a lytic substance released by the eggs
=Eggs passed in urine more during midday & discharged towards the end of micturition.
=Eggs laid in ectopic sites generally die and evoke local tissue reactions.
=May be found in rectal biopsies but are rarely passed live in feces

19
Q

S. haematobium hosts and infective form

A

=Definitive host: Humans are the only natural definitive hosts. No animal reservoir is known.
=Intermediate host:Fresh water snails Bulinus globossus.
=Infective form: Cercaria larva

20
Q

LIFE CYCLE AND TRANSMISSION OF S HAEMATOBIUM

A

①Eggs passed are embryonated & hatch in water to release the free living ciliated miracidia.
⓶Miracidia swim in water & penetrate into tissues of snail to reach its liver.
③Inside the snail,miracidia lose their cilia pass thru stages of the 1st & 2ndgeneration sporocysts to form cercariae(4–8 weeks).
④The cercariae(elongate ovoid body & forked tail) escape from the snail, swim about in water for 1–3 days.
⑤Upon contact with persons in water,they penetrate thru the skin facilitated by lytic substances secreted by penetration glands in the cercaria

21
Q

DEVELOPMENT IN MAN

A

⑥The cercariae shed their tails, become schistosomulae which enter the peripheral venules.
⑦The schistosomulae grow in intrahepatic portal veins & become sexually differentiated.
⑧They migrate to the vesical & pelvic venous plexuses where they mature, mate & begin laying eggs

22
Q

Evasion of host immune reaction of S. haematobium

A

①Avoidance of recognition by antibodies
Antigenic masking with “self ” antigens. ⓶Schistosomulae acquire host antigens eg.MHC antigens - sequestration

23
Q

Pathogenicity & Clinical Features of S. haematobium

A

Classified as follows based on stages in the evolution of the infection:
①Skin penetration and incubation period
⓶Egg deposition and extrusion
③Tissue proliferation and repair

24
Q

Skin penetration/incubation period of S. haematobium

A

=Cercarial dermatitis or general anaphylactic or toxic symptoms.
*Cercarial dermatitis consists of transient itching & petechial lesions at the site of entry of the cercariae (swimmer’s itch).
*Its particularly severe when infn is due to cercariae of nonhuman schistosomes.

=Anaphylactic/toxic symptoms include fever, headache, malaise & urticaria.
*This is accompanied by leucocytosis, eosinophilia, enlarged tender liver & a palpable spleen.
*This condition is more common in infection with S. japonicum (Katayama fever).

25
Q

Egg deposition and extrusion of S. haematobium

A

=Painless terminal hematuria, initially microscopic, but becomes gross, if infn is heavy.
=Most patients develop frequency of urination & burning sensation.
=Areas of hyperplasia & inflammation of bladder mucosa are seen on Cystoscopy.

26
Q

Tissue proliferation and repair in S. haematobium, infection

A

=Generalized hyperplasia & fibrosis of bladder mucosa with a granular appearance (sandy patch).
=Pseudo abscesses at sites of egg deposition due to infiltration by lymphocytes & eosinophils.
=Ulceration with secondary bacterial infection leading to chronic cystitis.
=Deposition of oxalate/uric acid crystals around the eggs & blood clots lead to calculi(stones) in the bladder.
=Obstructive hyperplasia of the ureters & urethra (hydroureter) may occur.
=Squamous cell carcinoma of the bladder occur in chronic schistosomiasis & in younger age group.
***S. haematobium is classified as a human carcinogen.

27
Q

Diagnosis of S. haematobium

A

=Demonstration of characteristic eggs in centrifuged urine deposits.
*Filtration of known volume with nucleopore is used for quantification for txt monitoring
*Occasionally eggs demonstrated in feces
=Histopathology by demonstrating eggs in
bladder mucosal biopsy.
=Detection of specific schistosome antigens(Adult gut Ag-circulating anodic antigen (CAA) & circulating cathodic antigens (CCA) serum/urines.
=Imaging- USG may show hydroureter & hydronephrosis.

28
Q

TREATMENT OF S. HAEMATOBIUM INFECTION

A

=Praziquantel (drug of choice).
=Metrifonate (alternative drug of choice in schistosomiasis due to S. haematobium).
=In secondary bacterial infn-antibiotics
=Neoplasms -surgical intervention is indicated

29
Q

Schistosoma japonicum infection and habitat

A

=Also referred to as Oriental blood fluke or Oriental schistosomiasis.

Habitat:
=Adult worms seen in the venules of the superior mesenteric vein & intrahepatic portal venules.

30
Q

Epidemiology and Transmission of S.japonicum

A

=Found in the far east-Japan , China ,Taiwan, Philippines.

=Zoonosis – cats,dogs, oxen, rats, mice, sheep, water buffalo, pigs, horses can also be infected
=Extensive use of night soil
=Small operculate snail intermediate host is amphibious, survive dry period with viable infection
*Eggs survive winters

31
Q

Morphology of S. japonicum

A

Similar to other schistosomes with a few differences.
=Males: slender with no integument tuberculations.

=Females: gravid female uterus contains 100 eggs & up to 3,500 eggs may be passed daily by a single worm.
=Eggs smaller & spherical with a lateral small rudimentary knob.

32
Q

Hosts and infective form of S. japonicum

A

=Definitive host: Man

=Intermediate host: Amphibious snail of genus
Oncomelania.

=Infective form: fork-tailed cercaria

33
Q

Life Cycle of S. japonicum

A

①Eggs deposited in venules penetrate the gut wall & passed in feces.
⓶Eggs hatch in water & miracidia infect the intermediate snails of the genus Oncomelania.
③The fork-tailed cercaria escaping from the snails is the infective form for men & other definitive hosts.

34
Q

Pathogenesis of S. japonicum infection

A

=Similar to S. mansoni in being intestinal
=Pathology more pronounced – as more eggs are produced.
=In acute phase of the disease, Katayama fever is similar to that seen in S. mansoni
=Intestinal disease manifests as colicky abdominal pain, bloody diarrhoea and anemia.

=In chronic illness, hepatosplenic & manifestations of portal hypertension(esophageal varices & GIT bleeding) are seen.
*Liver is maximally affected.
*Initial hepatomegaly occur followed by periportal fibrosis (clay pipe stem fibrosis).
*Secondary spleen enlargement occur.

35
Q

‘Katayama fever‘

A

=The acute phase of moderate or heavy infection with schistosomes may present as a febrile reaction with hyper eosinophilia that can last for several days or weeks.
=’Katayama fever; which is commonest in infection with Schistosoma japonicum, less common with S. mansoni and rarely seen with S. haematobium, appears with the onset of oviposition.
=It results from the formation and circulation of antigen-antibody immune complexes. which provoke a type of serum sickness and may be complicated by glomerulonephritis.

36
Q

Treatment of S. japonicum infection

A

Similar to that of S. mansoni.
Treatment
=S. japonicum infection is more resistant to treatment than other schistosomiasis
=Praziquantel is the drug of choice

37
Q

Schistosoma Mekongi Epidermiology, Infection and hosts

A

=Found in Thailand & Malaysia along the Mekongi river. It’s a Zoonosis
=It is closely related to S. japonicum but are slightly smaller & round.
=Man & dog are the definitive host
=Snail intermediate host: Lithoglyphopsis aperta, non amphibious
=Hepatosplenomegaly and ascites are the common clinical finding

38
Q

Schistosoma Intercalatum Epidermiology and infection

A

=This specie is found in West & Central Africa- Gabon, Cameroon, Congo, Zaire
=Eggs similar to S.hematobium but passed exclusively in stools.
=Intermediate host is Bulinus globossus in Zaire, Bulinus forskali, in Cameroon,

=Clinical Effects: Milder than S. mansoni
=Diagnosis is established by detection of the egg in feces and rectal biopsy.
=Praziquantel is the drug of choice.

39
Q

Other Schistosomes

A

=Schistosoma Matthei -sheep
South, Central and West Africa

=Schistosoma rodhain: rodents cats dogs more
virulent-human reports Zaire

=Schistosoma bovis - cattle
African: Authentic cases few

40
Q

PREVENTION & CONTROL

A

Three main measures are used.

  1. Snail control & eradication
  2. Sanitary improvement of the environment
  3. Treatment
    Health education