Distribution, transmission and infection:
The distribution of hookworm (Necator americanus and Ancylostoma duodenale) is worldwide, with particular prevalence in rural areas of the moist tropics where there is inadequate sanitation and people walk barefoot.
Four essential factors in the spread of hookworm are:
The two species produce indistinguishable thin-walled eggs that hatch in soil. Infection is usually acquired by walking barefoot in soil contaminated with human faeces. The larvae undergo several moults before infective larvae are produced. These are capable of penetrating unbroken skin, and in this way they gain access to the bloodstream to begin a migratory phase similar to that of ascaris. When they reach the gut they attach by their mouthparts to the mucosa of the small intestine. The adult worms, which are about 1-cm long, are similar, but the buccal capsule of A. duodenale bears two pairs of teeth, whereas N. americanus has two so-called ‘cutting plates’. Unlike most nematodes, the tail of male hookworms has a membranous bursa used for attachment to the female during copulation.
Hookworms ingest blood and move from site to site in the gut mucosa, leaving behind small bleeding lesions. These two facts are responsible for the chief pathological manifestation of heavy infection with hookworms: iron deficiency anaemia.
Ancylostoma duodenale infection can also be acquired by humans orally, and, in some endemic regions, this is the primary means of transmission. Following ingestion, the filariform larva is swallowed and, molting twice en route, develops to sexual maturity in the small intestine.
Global spread of hookworm:
An estimated 72.5 million humans harbor Ancylostoma duodenale, the majority (59 million) in Asia. Some 384.3 million are infected with N. americanus worldwide, of which one million live in the United States.
Symptomatology:
The course of human hookworm disease can be divided into three phases:
Invasion commences when infective larvae penetrate human skin. Although little damage is inflicted upon superficial skin layers, host cellular reaction stimulated during blood vessel penetration may isolate and kill the larvae. Local irritation from invading larvae, combined with inflammatory reaction to accompanying bacteria, evokes an urticarial condition commonly known as ground itch.
The migration phase is the period during which larvae escape from capillary beds in the lung, enter the alveoli, and progress up the bronchi to the throat. This migration can produce severe hemorrhaging when large numbers of worms are involved; otherwise, a dry cough and sore throat may be the only symptoms. In areas where re-infection is continual, some filariform larvae of Ancylostoma duodenale, following penetration, may invade host skeletal musculature where they remain dormant, resuming development at a later time. While there has been no explanation for this phenomenon, it is known that dormancy can be caused by pregnancy with development resuming at the onset of parturition. These larvae subsequently may appear in breast milk, which then becomes a vehicle for transmission to breast-feeding infants.
Diagnosis:
Diagnosis based on clinical symptoms can be misleading because the same symptoms may result from nutritional deficiencies or from a combination of infection and such deficiencies. Positive diagnosis requires identification of eggs in the feces. For light infections, concentration-type diagnostic techniques, such as zinc sulfate flotation or several modifications of the formalin-ether method, are employed.
Meticulous care in identification of larvae is essential, especially from stools that are several days old, since the rhabditiform larvae of hookworms strongly resembles that of Strongyloides and even those of ruminant parasites (e.g., Trichostrongylus spp.), which occasionally infect humans.
Prevention:
Obvious precautions to prevent the spread of hookworm infection include:
References:
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A2142C, A2142G, A2143G, A926G, Adenovirus 40/41, AGA926-928TTC, Akkermansia muciniphila, Amoxicillin, Ancylostoma duodenale, Anti-gliadin IgA, Ascaris lumbricoides, b-Glucuronidase, Bacillus spp., Bacteroides fragilis, Bacteroidetes, Bifidobacterium spp., Blastocystis hominis, C. difficile, Toxin A, C. difficile, Toxin B, Calprotectin, Campylobacter, Candida albicans, Candida spp., Chilomastix mesnili, Citrobacter freundii, Citrobacter spp., Clarithromycin, Clostridia (class), Cryptosporidium, Cyclospora spp., Cytomegalovirus, Desulfovibrio spp., Dientamoeba fragilis, E. coli O157, Elastase-1, Endolimax nana, Entamoeba coli, Entamoeba histolytica, Enterobacter spp., Enterococcus faecalis, Enterococcus faecium, Enterococcus spp., Enterohemorrhagic E. coli (EHEC), Enteroinvasive E. coli/Shigella, Enterotoxigenic E. coli LT/ST, Eosinophil Activation Protein (EDN/EPX), Epstein-Barr Virus, Escherichia spp., Faecalibacterium prausnitzii, Firmicutes, Firmicutes:Bacteroidetes Ratio, Fluoroquinolones, Fusobacterium spp., Geotrichum spp., Giardia, Gluten Peptide, gyrA D91G, gyrA D91N, gyrA N87K, gyrB R484K, gyrB S479N, Helicobacter pylori, Klebsiella pneumoniae, Klebsiella spp., Lactobacillus spp., M. avium subsp. paratuberculosis, Methanobacteriaceae (family), Microsporidium spp., Morganella spp., Necator americanus, Norovirus GI/II, Occult Blood - FIT, PBP1A N562Y, PBP1A S414R, PBP1A T556S, Pentatrichomonas hominis, Prevotella spp., Proteus mirabilis, Proteus spp., Pseudomonas aeruginosa, Pseudomonas spp., Rhodotorula spp., Rodotorula spp., Roseburia spp., Salmonella, Secretory IgA, Shiga-like Toxin E. coli stx1, Shiga-like Toxin E. coli stx2, Staphylococcus aureus, Staphylococcus spp., Steatocrit, Streptococcus spp., Taenia spp., Tetracycline, Trichuris trichiura, Vibrio cholerae, Virulence Factor, babA, Virulence Factor, cagA, Virulence Factor, dupA, Virulence Factor, iceA, Virulence Factor, oipA, Virulence Factor, vacA, Virulence Factor, virB, Virulence Factor, virD, Yersinia enterocolitica, Zonulin
