Moniliformis moniliformis

In what is commonly known as "brain-jacking", the parasite induces a behavioral change in its intermediate host that increases the risk of predation for the host. It is thought that this behavioral change holds an evolutionary advantage for the parasite by increasing its chances of getting to its definitive host. When M. moniliformis infests its intermediate host, the cockroach species Periplaneta americana, it changes the cockroach's escape response. In one study, it was concluded that cockroaches infected by M. moniliformis took longer to respond to wind stimuli simulating the approach of a potential predator and displayed fewer escape responses implying that the parasite infection renders its intermediate host more vulnerable to predation by hindering its ability to detect and escape from its predator. It is thought that serotonin plays a role in upending the communication between giant interneurons and the thoracic interneurons and in turn hampers the escape response of the cockroach.^[5] In a similar study, the effects of parasitism on three Periplaneta species are studied. The results show that Periplaneta australasiae uses substrates differently and moves around less when infected with Moniliformis moniliformis.^[6] Another study concludes an increased vulnerability of infected Periplaneta americana due to increased phototaxis, more time spent moving (due to slower movement) and movement in response to light (uninfected cockroaches hesitated before moving).^[7]

As it requires consumption of raw infested beetles or cockroaches, human acanthocephaliasis is rare.

In 1888 in Italy, Salvatore Calandruccio [it] infected himself by ingesting larvae, reported gastrointestinal disturbances, and then shed the eggs in two weeks. This was the first report of the clinical manifestations of an M. moniliformis infestation in humans.

Calandruccio provided the first description of the clinical manifestations of acanthocephaliasis and similar accounts are found in the few case studies since; many of the patients described were asymptomatic. When they showed symptoms, they normally experienced abdominal pain, diarrhea, dizziness, edema, and anorexia.^[8] In some patients, giddiness has also been reported.^[1] In rodents, acanthocephaliasis is fatal and manifests itself through hemorrhaging and gastrointestinal disturbance.

The proper diagnosis of acanthocephaliasis in humans is made through fecal analysis, which, if the host is infested, should contain adult worms or eggs. To obtain the worms from the host, piperazine citrate, levamisole and bithionol can be administered to the patient.^[8]

Acanthocephaliasis is treated with anti-helminthics. There is considerable debate over the efficacy of anti-helminth drugs on this parasite but, so far, the drugs seem to be working. Pyrantel pamoate and ivermectin have been shown to be particularly effective in treating patients.^[8] Mebendazole and thiabendazole have also both been cited to work.^[5][9]

Because the only way of developing acanthocephaliasis is through ingesting the intermediate hosts, the most effective means of prevention is avoiding the consumption of uncooked beetles and cockroaches. This is especially difficult in children exhibiting pica and in areas with poor hygiene. Awareness campaigns on the risks of consuming infested beetles and cockroaches would be effective. Moreover, preventing entry of the intermediate hosts into the home, and especially the kitchen where it is at risk of getting into the food, would help curb the risk of becoming infested.^[10]