Trichinella spiralis

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Trichinella spiralis

 

 

 

Introduction

 

Trichinella spiralis was first seen by James Paget but was named and

described by his Pofessor, Richard Owen. The family Trichinellidae

contains only one single genus Trichinella and was originally thought

only to contain the one species, Trichinella spiralis, which causes

the serious and often fatal disease in man known as trichinosis

(trichinelosis). It is a parasite of carnivorous animals and is

especially common in rats and in swine fed on uncooked garbage and

slaughter house scraps, humans become infected by eating raw pork,

with sausages being the most common cause of infection. It is a

cosmopolitan parasite and prevalent in many European countries with

the highest interest being in China.

 

 

 

It is now thought that there are four varieties of this species that

exists worldwide;

 

Trichinella spiralis spiralis - temperate zone – high infectivity for

pigs, rats and man.

 

Trichinella spiralis nelsoni - Tropics - low infectivity for pigs and

rats and high infectivity for lions, hyenas.

 

Trichinella spiralis nativa - Arctic - low infectivity for pigs, found

in polar bears, resistant to freezing.

 

Trichinella spiralis pseudospiralis- New Zealand – low infectivity for

pigs, rats and mice.

 

 

 

Trichinella spiralis is a `domestic' parasitic nematode long

recognised to cause a zoonosis transmitted to man by the ingestion of

infected pork.

 

 

Life cycle

 

Infection in the definitive hosts is acquired by the hosts eating raw

or undercooked flesh e.g. pork, containing encapsulated larvae. (Diag.

4 & 6 & Fig. 7) Rats are probably the most highly infected `natural'

hosts and pigs become infected by eating infected pork scraps or

occasionally rats which inhabit their stalls. For man sausages are a

dangerous source of the parasite as a small fragment of infected pork,

(after mincing), may become widely distributed among a number of sausages.

 

Humans become infected by eating raw meat containing encysted larvae.

The cyst becomes digested and releases the larvae which invade the

intestinal mucosa. They develop and mate in the second day. By the

6th day of infection, the female adults deposit motile larvae which

are carried by the intestinal lymphatics or mesenteric venules to

other tissues in the body. The very active muscles, such as the

diaphragm, jaws, tongue, larynx and eyes, are invaded and the larvae

become encapsulated by the 21st day following infection. Calcification

of the cysts occurring as early as five months, but usually begins

after 6 –18 months. The cyst wall is derived from the host's muscle

fibre and the larvae remain viable for many years with no further

development occurring. When muscles are eaten by the definitive host,

sexual maturation in the intestinal phase, as explained earlier,

rapidly occurs.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Diagram 4. Diagram illustrating the life cycle of Trichinella spiralis

which is the causative agent of the disease trichinosis which is often

terminally fatal in man.

 

 

 

 

 

Morphology

 

The adult female worm is about 2-3mm long and 90mm in diameter. The

male is smaller measuring 1.2mm long by 60mm in diameter. (Diag. 5 &

Fig. 6)

 

 

 

The female adult worms are ovoviparous and up to 1500 larvae may be

released by a single worm.

 

 

 

 

 

 

 

Diagram 5. Diagram illustrating the morphology of the adult male and

female nematodes, Trichinella spiralis. The adult female measures

between 2 – 3cm long whilst the male worms are smaller in size

measuring approximately 1.2mm long.

 

 

 

 

 

 

 

 

 

 

Figure 6. Parasitic female of Trichinella spiralis. The adult female

worms penetrate the mucosa of the host where they liberate the larvae,

which are then carried in the bloodstream to the muscle where they encyst.

 

Clinical Disease

 

Symptoms during the intestinal phase may go unnoticed or may be

severe. Epidemics can result in outbreaks of gastro-enteritis, 2 to 7

days after the ingestion of raw pork. Diarrhoea with or without

abdominal pain may last for several weeks. Eosinophilia and fever

occur in most cases. Leucocytosis is common and hyperglobulinaemia is

characteristic. Myocytosis and circum orbital oedema are classic

signs. There can also be central nervous system involvement

 

 

 

Pathogenicity

 

The primary pathogenic effect of Trichinella comes from the

destruction of the striated muscle fibres in which it encysts. (Diag.

6 & Fig. 7) There can be neurological manifestations of trichinosis

and death may be ascribed to myocarditis, encephalitis or pneumonitis.

 

Laboratory diagnosis

 

Diagnosis of trichinosis depends on the clinical signs, such as

myalgia, periorbital oedema, fever and eosinophilia in a patient with

a history of eating pork or sausages.

 

 

 

Serological tests are available but may be negative if carried out

within 3 - 4 weeks post infection. Circulating antibodies to T.

spiralis appear from 2 – 4 weeks after infection. Redefined diagnostic

antigens for their detection are currently being developed. A simple

IFAT employing fragments of larvae as antigen is a useful diagnostic

tool. Latex tests with extracted larval antigens have also proved

valuable in the acute stage, during which high antibody titres develop.

 

 

 

 

 

Figure 6. Diagrammatic representation of the larvae encapsulated in

striated muscle. (Smyth, J.D, 1994)

 

 

 

 

Figure 7 . Encapsulated Trichinella spiralis larvae in the muscle of

the definitive hosts. Man becomes infected by eating infected raw meat.

 

 

 

 

Muscle biopsy is available with the muscle being digested in pepsin,

which frees the encapsulated larvae or by a simple device whereby the

muscle sample is compressed between 2 glass plates to make it

semi-transparent, allowing you to see any encapsulated larvae using a

`trichinoscope' (a simple magnifying system). (Fig. 7)

 

References

 

 

 

Murray, PR, Drew, WL, Koyayashi, GS & Thomson, JH: Medical

Microbiology. Mosby Books Inc., New York (1990)

 

 

 

Peters, W & Gilles, HM: Tropical Medicine & Parasitology. Wolfe

Medical Publications Ltd.

 

 

 

Jeffrey & Leach: Atlas of Medical Helminthology and Protozoology. E &

S Livingstone Ltd.

 

 

 

Ash, LR & Orihel, TC: Atlas of Human Parasitology. ASCP Press, Chicago.

 

 

 

Garcia, LS & Bruckner, DA: Diagnostic Medical Parasitology. Elsevior

Science Publishing Co. Inc.

 

 

 

Muller, R & Baker, JR: Medical Parasitology. Gower Medical Publishing.

 

 

 

Smyth, J.D: Introduction to Animal Parasitology. Cambridge University

Press (1994)

 

 

 

Snell, JJS, Farrell, ID & Roberts, C: Quality Control, Principles and

Practice in the Microbiology Laboratory. Public Health Laboratory

Service. ISBN 0 901 144 312.

 

 

 

Brown, VC. A Longitudinal study of the prevalence of intestinal

helminths in baboons (Papio doguera) from Tanzania. (1994) Thesis,

Liverpool.

 

 

 

 

 

I would like to thank the authors of the following web sites:

 

www.cdfound.to.it