Larva currens is also a cause of migratory pruritic eruptions but is marked by 1) migratory speed on the order of inches per hour 2) perianal involvement due to autoinfection from stool and 3) a wide band of urticaria. Cause
Hookworm eggs are shed in the infected dog (or other animal) feces to the ground and beach sand, where they then develop over a period of 1–2 weeks into the infectious larval form (filariform larvae). The filariform larvae can burrow through intact skin that comes into contact with soil or sand that is contaminated with feces. Although they are able to infect the deeper tissues of animals (through to the lungs and then the intestinal tract), humans are incidental hosts and the larvae are only able to penetrate the epidermis of the skin and thus create the typical wormlike burrows visible underneath the skin. These parasites apparently lack the collagenase enzymes required to penetrate through the basement membrane deeper into the dermal layers of the skin. Treatment
CLM can be treated in a number of different ways:

Systemic (oral) agents include albendazole   (trade name Albenza)  and ivermectin (trade name Stromectol). Another agent which can be applied either topically or taken by mouth is thiabendazole (trade name Mintezol), an anti-helminthic. Topical freezing agents, such as ethylene chloride or liquid nitrogen, applied locally can freeze and kill the larvae, but this method has a high failure rate because the larvae are usually located away from the site of the visible skin trails.
Adverse events
Serious adverse events, which can cause death and disability, include:
Severe infusion reaction
Cardiac arrest
Cytokine release syndrome
Tumor lysis syndrome, causing acute kidney injury
Infections
Hepatitis B reactivation
Other viral infections
Progressive multifocal leukoencephalopathy (PML) caused by JC virus reactivation
Invasive fungal infections 
Immune toxicity, with depletion of B cells in 70% to 80% of lymphoma patients
Pulmonary toxicity
Bowel obstruction and perforationTwo patients with systemic lupus erythematosus died of progressive multifocal leukoencephalopathy (PML) after being treated with rituximab. PML is caused by activation of JC virus, a common virus in the brain which is usually latent. Reactivation of the JC virus usually results in death or severe brain damage.At least one patient with rheumatoid arthritis developed PML after treatment with rituximab.Rituximab has been reported as a possible cofactor in a chronic hepatitis E infection in a person with lymphoma. Hepatitis E infection is normally an acute infection, suggesting the drug in combination with lymphoma may have weakened the bodys immune response to the virus.A major concern with continuous rituximab treatment is the difficulty to induce a proper vaccine response. This was brought into focus during the COVID-19 pandemic, where persons with multiple sclerosis and rituximab treatment had higher risk of severe COVID-19. In persons with rituximab treatment for multiple sclerosis, 9 of 10 patients with B cell counts of 40/µL or more developed protective levels of antibodies after vaccination with tozinameran. Mechanisms of action
The antibody binds to the cell surface protein CD20.