Paragonimus westermani

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Paragonimus westermani (Kerbert, 1878) Braun, 1899

(Figure 2-42)

ETYMOLOGY:Para = side-by-side and gonimus = gonads along with westerman = for Dr. Westerman the curator of the Zoo in Amsterdam who submitted the original specimens to Dr. Kerbert for identification.

SYNONYMS:Distoma westermani Kerbert, 1878; Distoma ringeri Cobbold, 1880; Distoma pulmonum Baelz, 1881; Distoma pulmonis Kiyona, 1881; Mesogonimus westermani Railliet, 1890; Polysarcus westermanni Lühe, 1899.

HISTORY:Paragonimus westermani was described as Distoma westermani for specimens that were recovered from Indian tigers that died in zoos in Amsterdam and Hamburg. At the same time parasites were observed by Drs. Manson, Ringer, and Cobbold that were described as a new species Distoma ringeri. Braun in 1899 created the genus Paragonimus in which he placed Paragonimus westermani.

GEOGRAPHIC DISTRIBUTION:Paragonimus westermani is found in southeastern Siberia, Japan and Korea through China, Taiwan, and the Philippines, through Indonesia, Malaysia, and Thailand, and into India and Sri Lanka.

LOCATION IN HOST: In cysts in the lungs.

PARASITE IDENTIFICATION: Species of Paragonimus are 7 to 12 mm long, 4 to 8 mm wide, and quite thick, i.e., 4 to 6 mm. Paragonimus westermani differs from other species of Paragonimus in Asia in that specimens of Paragonimus pulmonalis reproduce parthenogenetically and have no sperm in the seminal receptacle; specimens of Paragonimus miyazakii are more slender than Paragonimus westermani and Paragonimus pulmonalis, have a ventral sucker that is slightly larger than the oral sucker, and have more lobes on the ovary and testis; specimens of Paragonimus heterotremus have an oral sucker that is about twice the diameter of the ventral sucker (in most species they are approximately the same size); specimens of Paragonimus skrjabini tend to be more elongate with a tapered posterior end and the ventral sucker being somewhat anteriad; specimens of Paragonimus ohirai are characterized by having the spines on the body surface appearing in groups or clusters rather than being singularly spaced.

The eggs have a brown shell, a distinct operculum, and occasionally a knob on the abopercular end; eggs range from 70 to 100 µm in length by 39 to 55 µm in width.

In Korea, work has been performed that has shown that ELISAs using both crude and purified antigens of Paragonimuswestermani show promise for the identification of infections in cats (Lee and Chang, 1987; Choi et al., 1987). Specific antibody levels were significantly increased by two to three weeks after infection, and they remained elevated for up to 6 months. After treatment, specific antibody returned to baseline levels.

LIFE CYCLE: The adult flukes lay eggs that are coughed up with sputum and then swallowed to be passed in the feces. After the feces enters fresh water, it takes about 2 weeks for the eggs to mature and for the miracidium to hatch. The free swimming miracidium infects a species of snail within the genera Brotia or Semisulcospira. The second intermediate hosts are fresh-water crabs (Sinopotamon, Candidiopotamon, Sundathelphusa, Parathelphusa, Geohelphusa, and Ranguna) and crayfish (Cambaroides). The second intermediate hosts typically become infected when they eat the infected snail that harbors cercariae that are characterized by a very short tail and a pronounced stylet associated with the oral sucker. The metacercariae of Paragonimus westermani are slightly smaller than those of Paragonimus pulmonalis measuring about 0.35 mm in diameter; the metacercariae are found in the gills and the muscles. When ingested, the metacercariae migrate through the intestinal wall into the abdominal cavity. After several days in the abdominal cavity, the worms migrate through the diaphragm into the lungs where they develop to adult worms, typically in pairs. Infections become patent in 65 to 90 days, and in humans, patent infections have been maintained for up to 20 years. Pigs have been shown to serve as paratenic hosts, and it is possible that other smaller rodents may also serve in this fashion. In these hosts, the young flukes are found distributed throughout the muscle tissues.

CLINICAL PRESENTATION AND PATHOGENESIS: Infections in cats produce signs that are markedly less severe than infections with similar numbers of worms in human beings or other primates (Yokogawa et al., 1960). The young flukes appear to migrate about the abdominal cavity at random initially, causing hemorrhagic lesions in the liver and intestinal wall. Also, there are marked hemorrhagic lesions in the diaphragm, and at 20 to 30 days after infection, holes appear in the tendinous and at the edge of the muscular portions of the diaphragm that indicate the passage of larger flukes. Experimentally infected cats have died of hemorrhage into the pleural cavity. The lung parenchymal nodules that develop in cats are more clearly circumscribed than those that develop in human beings. In cats with heavy natural infections, there is extensive injury to the lung parenchyma, the pleura, and enlargement of the lymphatic tissues. The pleura becomes thickened and fibrotic and the lungs developed atelectasis and fibrosis. Eggs become widely scattered in the lung tissues and are present in the lymph nodes of the pleural cavity (Kau and Wu, 1936 [from Yokogawa, et al. 1960]). Cats infected with Paragonimus westermani may also have small numbers of eggs in other tissues including the cerebrum, cerebellum, and myocardium (Shigemi, 1957 [from Yokogawa et al., 1960]).

Paragonimus westermani differs from Paragonimus pulmonalis in that more than a single worm is required for the production of fertilized eggs. Thus, if a cat is infected with a single metacercaria of Paragonimus westermani, the young fluke will not mature and will often continue to migrate around in the pleural cavity laying eggs that are not capable of developing mature miracidia (Miyazaki, 1991). This might mean that cats with single worm infections are more likely to develop lesions in ectopic sites.

TREATMENT: A cat from mainland China was treated for Paragonimus westermani using praziquantel. The cat was passing 11,390 eggs per gram of feces prior to treatment, it was treated with 100 mg of praziquantel per kg daily for 2 days. No eggs were detected in the feces of the cat 15 and 30 days after treatment (Cao et al., 1984). Experimentally infected cats have also been successfully treated with praziquantel (Choi et al., 1987).

EPIZOOTIOLOGY: Numerous mammals are capable of being infected with Paragonimus westermani. The host that harbors the largest numbers of parasites is the tiger. In a survey performed in Sumatra, Indonesia, all of 10 tigers that were examined were infected, and 1 tiger had a total of 1,596 flukes in its lungs (Kwo and Miyazaki, 1968). Other hosts that have been naturally infected include dogs, foxes, pigs, raccoon-dogs, various members of the cat family, civets, mongoose, and crab-eating macaques.

HAZARD TO OTHER ANIMALS: If mammals ingest the infected crab, there is a possibility that larval flukes will penetrate the intestinal wall and migrate into the abdominal cavity. In permissive hosts, the flukes will go onto develop in the lungs while in some hosts the flukes will persist as in the swine paratenic host. In all these hosts, there is the possibility for associated pathology.

HAZARD TO HUMANS: Many human beings are infected with this parasite; infections are obtained by eating raw or undercooked crabs or meat of the seine paratenic host. Symptoms from the lung lesions can be severe. Similarly, the migration of worms to ectopic locations, such as the brain, can cause severe pathology. Cats are considered a major source of eggs in the environment.


Cao WJ, He LY, Zhong HL, Xu ZS, Bi YC, Yu GT, Zhang QC, Li KC, Yang EV, She G, Li HJ. 1984. Paragonimiasis: Treatment with praziquantel in 40 human cases and in 1 cat. Drug Res 34:1203-1204.

Choi WY, Yoo JE, Nam HW, Choi HR. 1987. Purification of antigenic proteins of Paragonimuswestermani and their applicability to experimental cat paragonimiasis. Kor J Parasitol 24:177-186.

Kwo EH, Miyazaki I. 1968. J Parasitol 54: NEED REFERENCE

Lee OR, Chang JK. 1987. ELISA of paragonimiasis in cat by crude and purified antigens of Paragonimuswestermani. Kor J Parasitol 24:187-193.

Miyazaki I. 1991. Helminthic Zoonoses. 494 pages. International Medical Foundation of Japan. Fukuoka, Japan.

Yokogawa S, Cort WW, Yokogawa M. 1960. Paragonimus and Paragonimiasis. Exp Parasitol 10:81-205.

Figure 2-42.Paragonimuswestermani from the lung of a human.

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