Mansonella perstans

Mansonella perstans is a vector-borne human filarial nematode, transmitted by tiny blood-sucking flies called midges. Mansonella perstans is one of two filarial nematodes that causes serous cavity filariasis in humans. The other filarial nematode is Mansonella ozzardi. M. perstans is widespread in many parts of sub-Saharan Africa, parts of Central and South America, and the Caribbean. Compared to infections with other filarial parasites such as Wuchereria bancrofti, Brugia malayi, and Loa loa, Mansonella infections are relatively mild. However, the pathogenicity of M. perstans infection has been recently reconsidered in various studies. These studies have demonstrated that M. perstans has the ability to induce a variety of clinical features, including angioedema Calabar-like swellings, pruritus, fever, headache, eosinophilia, and abdominal pain. The overall disability among populations in regions where filariae are endemic has been difficult to determine because of high rates of coinfection with other filariae and the nonspecificity of M. perstan infections. Furthermore, treatment of M. perstans is challenging because the most antifilarial drugs, such as ivermectin, diethylcarbamazine, and albendazole are not effective. The optimal treatment for M. perstans infection remains unclear. Most current studies are focused on coinfection of M. perstans with other filarial parasites, and the study of Wolbachia bacteria as endosymbionts in M. perstans and other filarial parasites. In 1890, the microfilariae of M. perstans were first discovered by Manson in the blood of a patient from West Africa who was hospitalized with sleeping sickness in London. Because the microfilariae were first noted in a patient with African trypanosomiasis, M. perstans was initially suspected to be the cause of this disease. M. perstans as the cause of African trypanosomyasis was later ruled out by the Royal Society Sleeping Sickness Commission, who showed the geographical distribution of sleeping sickness did not coincide with that of M. perstans infection. Upon their discovery, the microfilariae were named Filaria sanguinis hominis minor, due to their relatively small size when compared to another type of microfilarae found in the same patient (Filaria sanguinis hominis major, which is now known as Loa loa). The name was later changed to Filaria sanguinis hominis perstans, and later again shortened to Filaria perstans to comply with the binary system of nomenclature. Over time, the name continued to change as changes in the generic status of the parasite took place. In 1984, Eberhard and Orihel redefined the genus Mansonella and included the M. perstans species in it, so it is currently known as M. perstans. The adult worms of M. perstans were first recovered during post mortem examination of two aboriginal Indians in British Guiana from their mesentery and subpericardial fat. While an insect vector was hypothesized, it took many years of investigation before the true vector of M. perstans was discovered. While Mansonella infections are often asymptomatic, they can be associated with angioedema (similar to Calabar swellings of loaisis), recurrent pruritic subcutaneous lesions, fever, headaches, arthralgia, and neurologic manifestations. Eosinophilia, headache, fever, or abdominal pain may also be present. M. perstans may also present with a condition known as kampala, or Ugandan eye worm. This occurs when adult worms of M. perstans invade the conjunctiva or periorbital connective tissues in the eye. This condition was first attributed to M. perstans in Uganda, when six patients presented with nodules in the conjunctiva. The adult worms were identified as adult female M. perstans in five of these six cases. The symptoms of M. perstans may be confounded with those of other filarial infections, such as onchocerciasis, lymphatic filariasis and loiasis, because coinfection often occurs. A 36-year-old man was admitted to the outpatient clinic at the Goundi Missionary Hospital in the south of Chad in May 2001. He complained of visual impairment in the left eye, ocular and abdominal pruritus, and abdominal pain. He had previously been treated with DEC for M. perstans infection five months prior to his visit. A blood sample was taken at 11:00 am, and examined microscopically as a thick blood film stained with Giemsa's solution. The thick blood film revealed the presence of M. perstans, and no other parasites were found. He had 3% eosinophilia. A visual acuity test showed a reduction of visual acuity to 4/10 for the left eye, while the right eye was 9/10. However, no abnormalities were observed during examination of the anterior left eye chamber. Upon examination of the fundus of his left eye, a narrow, white, motionless, and linear lesion of 6–7 mm was found. He was then treated with a second course of DEC (400 mg daily in two doses for eight days, after a three-day dosage increase), and by the end of treatment, he did not have pruritus, but his visual impairment was unchanged. The M. perstans burden was significantly reduced, and the peripheral eosinohpil count decreased to 1%. He was then treated with mebendazole (100 mg twice a day, for 14 days), and at the end of his treatment, his visual impairment was the only symptom remaining. After a week, with no further treatment, his vision improved and acuity was increased to 8/10 in the left eye. While ocular symptoms occur quite frequently in symptomatic M. perstans infection, intraocular localization had not been described prior to this study. This case also is an example of the difficulty of treating mansonelliasis, and shows that combined drug regimens can be more effective than treatment using a single drug. M. perstans might potentially interfere with the host's regulatory mechanisms and influence the outcome of other infections, such as malaria, tuberculosis and HIV, which often thrive in similar environments.