Scabies

Infectious Disease MONDO:0004525 Pathograph 11 Show in embeddings browser Parasitic infection Neglected tropical disease

Scabies is a contagious parasitic skin disease caused by infestation of the stratum corneum by the burrowing ectoparasitic mite Sarcoptes scabiei var. hominis. Mite burrowing and release of antigenic metabolites trigger host innate and adaptive immune responses involving epidermal keratinocytes, dermal fibroblasts, T lymphocytes, eosinophils, and mast cells, with features of both type I and delayed type IV hypersensitivity, manifesting clinically as intense pruritus and an inflammatory papulovesicular skin rash in ordinary scabies or severe hyperkeratotic crusted plaques in crusted scabies.

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Classifications

Harrison's Part
INFECTIOUS DISEASES DERMATOLOGY
◆

Subtypes

2
Ordinary Scabies
Classic clinical presentation in immunocompetent hosts characterized by a low mite burden and a protective CD4+ T-cell-dominated Th1 cell-mediated immune response, manifesting as burrows, erythematous papules, and intense pruritus.
Show evidence (2 references)
PMID:34925353 SUPPORT BACKGROUND Human clinical
"However, various studies have consistently shown that the immune response of the host to ordinary scabies is a Th1 cell-mediated protective type and to the crusted variety of the scabies is a non-protective Th2 allergic response (6, 17, 18)."
Establishes that ordinary scabies elicits a protective Th1 cell-mediated host immune response distinct from crusted scabies.
PMID:34925353 SUPPORT BACKGROUND Human clinical
"CD4+ T cells mostly dominate the infiltrates of skin biopsy lesions in ordinary scabies, with a 4:1 ratio of CD4+ to CD8+ T cells (12, 13)."
Documents the CD4+ T-cell dominance (4:1 CD4+:CD8+ ratio) in skin lesions of ordinary scabies.
Crusted (Norwegian) Scabies
Severe, highly contagious form of scabies occurring predominantly in immunocompromised or elderly individuals, characterized by a non-protective Th2 allergic immune response (elevated IL-4, IL-5, IL-13, and IgE) with dermal CD8+ T-cell predominance, exuberant hyperkeratotic crusted lesions harboring abundant mites, and requirement for prolonged combination therapy.
Show evidence (3 references)
PMID:30755943 SUPPORT Human clinical
"A more severe form called crusted or Norwegian scabies may occur in immunosuppressed patients and the elderly. Crusted scabies mostly differs from normal scabies by the exuberance of its lesions, body distribution and high contagiousness, and requires different and more prolonged treatment."
Defines crusted (Norwegian) scabies, its predilection for immunosuppressed and elderly hosts, exuberant lesions, high contagiousness, and distinct treatment needs.
PMID:34925353 SUPPORT BACKGROUND Human clinical
"However, various studies have consistently shown that the immune response of the host to ordinary scabies is a Th1 cell-mediated protective type and to the crusted variety of the scabies is a non-protective Th2 allergic response (6, 17, 18). In addition, Crusted Scabies (CS) patients have shown..."
Characterizes the non-protective Th2 cytokine profile (increased IL-4, IL-5, and IL-13 with reduced IFN-gamma) in crusted scabies.
PMID:34925353 SUPPORT BACKGROUND Human clinical
"In comparison, the skin inflammatory response in patients with crusted scabies predominantly comprises CD8+T cells (6, 12)."
Documents CD8+ T-cell predominance in the cutaneous inflammatory infiltrate of crusted scabies.
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Pathophysiology

5
Mite infestation of the skin
Sarcoptes scabiei var. hominis burrows into the stratum corneum of human epidermis and feeds on host epidermis and sera, releasing antigenic saliva, fecal pellets, and active metabolites that disrupt the epidermal barrier and initiate host cutaneous inflammatory and immune responses.
keratinocyte CL:0000312 Cell Ontology (CL) Relation: this pathophysiological event involves this cell type This pathophysiological event involves keratinocyte (CL:0000312). CL:0000312 is a cell type from the Cell Ontology.
stratum corneum of epidermis UBERON:0002027 Uberon multi-species anatomy ontology (UBERON) Relation: this pathophysiological event occurs in this anatomical location This pathophysiological event occurs in stratum corneum of epidermis (UBERON:0002027). UBERON:0002027 is an anatomical location from the Uberon multi-species anatomy ontology. skin epidermis UBERON:0001003 Uberon multi-species anatomy ontology (UBERON) Relation: this pathophysiological event occurs in this anatomical location This pathophysiological event occurs in skin epidermis (UBERON:0001003). UBERON:0001003 is an anatomical location from the Uberon multi-species anatomy ontology.
Downstream
Keratinocyte and Fibroblast Cytokine and Keratinization Response Burrowing mites and secreted mite antigens directly stimulate resident epidermal keratinocytes and dermal fibroblasts.
Dermal Leukocyte and Granulocyte Infiltration Mite products and keratinocyte/fibroblast chemokines recruit neutrophils, macrophages, T lymphocytes, eosinophils, and mast cells into the dermis.
Show evidence (2 references)
PMID:34925353 SUPPORT BACKGROUND Human clinical
"S. scabiei var. hominis causes skin infestation in humans by forming burrows in the stratum corneum of the skin and feeding on host epidermis and sera. The release of active metabolites from the mite contribute to the intense itching and inflammation manifesting as a skin allergy and..."
Describes burrow formation in the stratum corneum, feeding on host epidermis and sera, and release of antigenic mite saliva, fecal material, and enzymes.
PMID:30755943 SUPPORT Human clinical
"Scabies is an infestation of the skin by the mite Sarcoptes scabiei."
Confirms cutaneous infestation by S. scabiei.
Keratinocyte and Fibroblast Cytokine and Keratinization Response
Epidermal keratinocytes and dermal fibroblasts respond to burrowing mites by upregulating innate proinflammatory cytokines and chemokines (including IL1A, IL1B, and CXCL8) alongside epidermal development and keratinization gene programs (including KRT6C, KRT9, SPRR2A, SPRR3, and LCE3A).
keratinocyte CL:0000312 Cell Ontology (CL) Relation: this pathophysiological event involves this cell type This pathophysiological event involves keratinocyte (CL:0000312). CL:0000312 is a cell type from the Cell Ontology. fibroblast CL:0000057 Cell Ontology (CL) Relation: this pathophysiological event involves this cell type This pathophysiological event involves fibroblast (CL:0000057). CL:0000057 is a cell type from the Cell Ontology.
IL1A hgnc:5991 HUGO Gene Nomenclature Committee (hgnc) Relation: this pathophysiological event involves this gene This pathophysiological event involves IL1A (hgnc:5991). hgnc:5991 is a gene from the HUGO Gene Nomenclature Committee. IL1B hgnc:5992 HUGO Gene Nomenclature Committee (hgnc) Relation: this pathophysiological event involves this gene This pathophysiological event involves IL1B (hgnc:5992). hgnc:5992 is a gene from the HUGO Gene Nomenclature Committee. CXCL8 hgnc:6025 HUGO Gene Nomenclature Committee (hgnc) Relation: this pathophysiological event involves this gene This pathophysiological event involves CXCL8 (hgnc:6025). hgnc:6025 is a gene from the HUGO Gene Nomenclature Committee.
keratinization GO:0031424 ↑ INCREASED Gene Ontology (GO) Relation: this pathophysiological event involves this biological process This pathophysiological event involves increased keratinization (GO:0031424). GO:0031424 is a biological process from the Gene Ontology. inflammatory response GO:0006954 ↑ INCREASED Gene Ontology (GO) Relation: this pathophysiological event involves this biological process This pathophysiological event involves increased inflammatory response (GO:0006954). GO:0006954 is a biological process from the Gene Ontology.
skin epidermis UBERON:0001003 Uberon multi-species anatomy ontology (UBERON) Relation: this pathophysiological event occurs in this anatomical location This pathophysiological event occurs in skin epidermis (UBERON:0001003). UBERON:0001003 is an anatomical location from the Uberon multi-species anatomy ontology. dermis UBERON:0002067 Uberon multi-species anatomy ontology (UBERON) Relation: this pathophysiological event occurs in this anatomical location This pathophysiological event occurs in dermis (UBERON:0002067). UBERON:0002067 is an anatomical location from the Uberon multi-species anatomy ontology.
Downstream
Dermal Leukocyte and Granulocyte Infiltration Keratinocyte and fibroblast cytokines and chemokines (including IL-1alpha, IL-1beta, and CXCL8) recruit neutrophils, macrophages, T cells, and eosinophils to the dermis.
JAK-STAT Signaling Pathway Activation Secreted epidermal and dermal cytokines engage cell-surface receptors to activate intracellular JAK-STAT signaling cascades in lesional skin.
Hyperkeratosis Sustained upregulation of epidermal keratinization programs and keratinocyte-derived IL-20 signaling drives epidermal thickening, scaling, and hyperkeratotic crust formation in crusted scabies.
Show evidence (3 references)
PMID:23940705 SUPPORT PRIMARY RESULT In vitro / ex vivo
"Genes for the expression of interleukin-1α (IL-1α) precursor, IL-1β, granulocyte/macrophage-colony stimulating factor (GM-CSF) precursor, and G-CSF precursor were up-regulated 2.8- to 7.4-fold, paralleling cytokine secretion profiles. A large number of genes involved in epithelium development..."
Demonstrates upregulation of IL1A, IL1B, and keratinization gene programs in human skin equivalents (keratinocytes and fibroblasts) challenged with live burrowing S. scabiei mites.
PMID:34925353 SUPPORT PRIMARY RESULT Human clinical
"Top upregulated genes displayed a role in inflammatory responses and innate immunity (DEFB4A, IL-19, CXCL8, CSF3, SERPINB4, S100A7A, HRNR), keratinization (KRT9, KRT6C, EGR4, SPRR3, LCE3A, SPRR2A, LCE3A), and a gene involved in desquamation processes in skin (SPINK9);"
Human scabies skin biopsy RNA-seq confirms strong upregulation of CXCL8 and keratinization genes.
PMID:34925353 SUPPORT PRIMARY RESULT Human clinical
"As expected, the results showed that pathways associated with skin development, including keratinization, epidermis development, and keratinocyte differentiation, were highly upregulated in the diseased samples."
Pathway enrichment analysis of human scabies lesions confirms upregulation of keratinization and keratinocyte differentiation.
Dermal Leukocyte and Granulocyte Infiltration
Recruitment and accumulation of T lymphocytes, macrophages, neutrophils, eosinophils, and mast cells in the dermis. In ordinary scabies, CD4+ T lymphocytes predominate in a 4:1 ratio over CD8+ T cells as part of a protective Th1 cell-mediated response, whereas crusted scabies exhibits dermal CD8+ T-cell predominance alongside heavy eosinophil, lymphocyte, and macrophage infiltration.
T cell CL:0000084 Cell Ontology (CL) Relation: this pathophysiological event involves this cell type This pathophysiological event involves T cell (CL:0000084). CL:0000084 is a cell type from the Cell Ontology. macrophage CL:0000235 Cell Ontology (CL) Relation: this pathophysiological event involves this cell type This pathophysiological event involves macrophage (CL:0000235). CL:0000235 is a cell type from the Cell Ontology. eosinophil CL:0000771 Cell Ontology (CL) Relation: this pathophysiological event involves this cell type This pathophysiological event involves eosinophil (CL:0000771). CL:0000771 is a cell type from the Cell Ontology. mast cell CL:0000097 Cell Ontology (CL) Relation: this pathophysiological event involves this cell type This pathophysiological event involves mast cell (CL:0000097). CL:0000097 is a cell type from the Cell Ontology. neutrophil CL:0000775 Cell Ontology (CL) Relation: this pathophysiological event involves this cell type This pathophysiological event involves neutrophil (CL:0000775). CL:0000775 is a cell type from the Cell Ontology.
leukocyte chemotaxis GO:0030595 ↑ INCREASED Gene Ontology (GO) Relation: this pathophysiological event involves this biological process This pathophysiological event involves increased leukocyte chemotaxis (GO:0030595). GO:0030595 is a biological process from the Gene Ontology. immune response GO:0006955 ↑ INCREASED Gene Ontology (GO) Relation: this pathophysiological event involves this biological process This pathophysiological event involves increased immune response (GO:0006955). GO:0006955 is a biological process from the Gene Ontology.
dermis UBERON:0002067 Uberon multi-species anatomy ontology (UBERON) Relation: this pathophysiological event occurs in this anatomical location This pathophysiological event occurs in dermis (UBERON:0002067). UBERON:0002067 is an anatomical location from the Uberon multi-species anatomy ontology.
Downstream
Type 2 Cytokine and IL-31 Pruritogenic Signaling Infiltrating T cells, eosinophils, and mast cells secrete type 2 and pruritogenic cytokines including IL-4, IL-13, and IL-31.
Skin rash Combined type I and delayed type IV dermal cellular infiltration produces erythematous papules and inflammatory skin lesions.
Show evidence (2 references)
PMID:34925353 SUPPORT BACKGROUND Human clinical
"Upon recruitment to infection site/draining lymph nodes, eosinophils, mast cells, and basophils produce IL-4 and /or IL-13 (10). In a study reported by Walton et al. in 2008, skin biopsies taken from scabies patients having crusted lesions showed large numbers of lymphocytes, monocytes,..."
Documents recruitment of eosinophils, mast cells, lymphocytes, monocytes, and macrophages into the dermis of scabies lesions.
PMID:34925353 SUPPORT BACKGROUND Human clinical
"The immune response to S. scabiei consistently shows increased levels of CD4+ or CD8+ T cells. CD4+ T cells mostly dominate the infiltrates of skin biopsy lesions in ordinary scabies, with a 4:1 ratio of CD4+ to CD8+ T cells (12, 13)."
Demonstrates dermal T-cell infiltration with CD4+ T-cell dominance in ordinary scabies and CD8+ T-cell involvement.
JAK-STAT Signaling Pathway Activation
Transcriptional and functional upregulation of the intracellular JAK-STAT signaling cascade in scabies-infested skin, promoting macrophage and neutrophil activation, B- and T-lymphocyte differentiation, and amplification of cytokine-mediated cutaneous inflammation.
cell surface receptor signaling pathway via JAK-STAT GO:0007259 ↑ INCREASED Gene Ontology (GO) Relation: this pathophysiological event involves this biological process This pathophysiological event involves increased cell surface receptor signaling pathway via JAK-STAT (GO:0007259). GO:0007259 is a biological process from the Gene Ontology.
skin of body UBERON:0002097 Uberon multi-species anatomy ontology (UBERON) Relation: this pathophysiological event occurs in this anatomical location This pathophysiological event occurs in skin of body (UBERON:0002097). UBERON:0002097 is an anatomical location from the Uberon multi-species anatomy ontology.
Downstream
Type 2 Cytokine and IL-31 Pruritogenic Signaling JAK-STAT pathway activation transduces and amplifies IL-4, IL-13, and IL-31 cytokine signaling in lesional skin.
Show evidence (2 references)
PMID:34925353 SUPPORT PRIMARY RESULT Human clinical
"The clustering patterns showed various differentially expressed genes including inflammatory responses and innate immunity genes (DEFB4A, IL-19, CXCL8, CSF3, SERPINB4, S100A7A, HRNR) and notably upregulation of the JAK-STAT pathway in scabies-infested samples."
Bulk RNA-seq of human scabies skin biopsies identifies prominent upregulation of the JAK-STAT signaling pathway.
PMID:34925353 SUPPORT BACKGROUND Human clinical
"Differentially expressed genes that were enhanced in OS included immune-related signaling pathways and JAK-STAT pathways. Their impacts include activation of macrophages and neutrophils, host inflammatory responses, and the differentiation of B and T cells, which control the wound repair (67)."
Details the functional consequences of JAK-STAT pathway activation in ordinary scabies skin lesions.
Type 2 Cytokine and IL-31 Pruritogenic Signaling
Upregulation of type 2 cytokines (IL4, IL13) and the pruritogenic cytokine IL31, alongside Th2-associated chemokines (CCL17, CCL18), in mite-infested skin. IL-4 sensitizes pruriceptors to histamine and IL-31 signals to induce severe pruritus, with expression levels correlating directly with clinical itch severity scores.
T cell CL:0000084 Cell Ontology (CL) Relation: this pathophysiological event involves this cell type This pathophysiological event involves T cell (CL:0000084). CL:0000084 is a cell type from the Cell Ontology. eosinophil CL:0000771 Cell Ontology (CL) Relation: this pathophysiological event involves this cell type This pathophysiological event involves eosinophil (CL:0000771). CL:0000771 is a cell type from the Cell Ontology. mast cell CL:0000097 Cell Ontology (CL) Relation: this pathophysiological event involves this cell type This pathophysiological event involves mast cell (CL:0000097). CL:0000097 is a cell type from the Cell Ontology.
IL4 hgnc:6014 HUGO Gene Nomenclature Committee (hgnc) Relation: this pathophysiological event involves this gene This pathophysiological event involves IL4 (hgnc:6014). hgnc:6014 is a gene from the HUGO Gene Nomenclature Committee. IL13 hgnc:5973 HUGO Gene Nomenclature Committee (hgnc) Relation: this pathophysiological event involves this gene This pathophysiological event involves IL13 (hgnc:5973). hgnc:5973 is a gene from the HUGO Gene Nomenclature Committee. IL31 hgnc:19372 HUGO Gene Nomenclature Committee (hgnc) Relation: this pathophysiological event involves this gene This pathophysiological event involves IL31 (hgnc:19372). hgnc:19372 is a gene from the HUGO Gene Nomenclature Committee.
type I hypersensitivity GO:0016068 ↑ INCREASED Gene Ontology (GO) Relation: this pathophysiological event involves this biological process This pathophysiological event involves increased type I hypersensitivity (GO:0016068). GO:0016068 is a biological process from the Gene Ontology.
skin of body UBERON:0002097 Uberon multi-species anatomy ontology (UBERON) Relation: this pathophysiological event occurs in this anatomical location This pathophysiological event occurs in skin of body (UBERON:0002097). UBERON:0002097 is an anatomical location from the Uberon multi-species anatomy ontology.
Downstream
Pruritus Elevated IL-4, IL-13, and IL-31 in lesional skin directly stimulate and sensitize cutaneous sensory nerve fibers to produce intense pruritus.
Show evidence (3 references)
PMID:34925353 SUPPORT PRIMARY RESULT Human clinical
"DEGs in scabies mite-infested skin included those encoding certain chemokines (C-C motif) ligands CCL2, CCL17, and CCL 18, (C-X-C motif) ligand CXCL1, IL-17A, IL-17F, IL-23, IL-31 with FC greater than two for most of the genes. IL-4, CCL7, CCL20, IL-19, IL-20, IL-36A were also prominent DEGs..."
Demonstrates significant upregulation of IL31 and IL4 in human scabies lesions and correlation of IL4 with clinical itch severity scores.
PMID:34925353 SUPPORT PRIMARY RESULT Human clinical
"Marked enrichment of immune response pathways (JAK-STAT signaling, IL-4 and IL-13 pathway, and Toll receptor cascade), chemokine ligands and receptors (CCL17, CCL18, CCL3L1, CCL3L3, CCR7), and cytokines (IL-13 and IL-20) were observed."
Confirms enrichment of the IL-4 and IL-13 pathway and upregulation of IL13 in human scabies lesions.
PMID:34925353 SUPPORT BACKGROUND Human clinical
"IL-4 and IL-31 were also significantly high in scabies mite-infested skin. IL-4 is reported to increase the itching even in low dose of histamine (91), and IL-31 is known to be involved in causing itching by signal activation of IL-13 receptors, but the mechanism involved is still unclear (92)."
Explains how elevated IL-4 and IL-31 in scabies-infested skin drive itching through histamine sensitization and receptor signaling.
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Pathograph

Use Group by to collapse related nodes into one box. Use the checkboxes to hide or show graph categories. Hover nodes for evidence and cross-linked metadata.
Pathograph: causal mechanism network for Scabies Interactive directed graph showing how pathophysiology mechanisms, phenotypes, genetic factors and variants, experimental models, environmental triggers, and treatments relate through causal and linked edges.
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Phenotypes

4
Immune 2
Skin rash VERY_FREQUENT HP:0000988 Human Phenotype Ontology (HP) Relation: this clinical feature is this phenotype This clinical feature is Skin rash (HP:0000988). HP:0000988 is a phenotype from the Human Phenotype Ontology.
Sequelae: Recurrent bacterial skin infections
Show evidence (2 references)
PMID:34925353 SUPPORT BACKGROUND Human clinical
"Infestation by the mite almost always leads to the development of localized skin inflammation, itching, and burrow formation; rash and itch possibly being an indicator of host immune response with features of both type I and type IV hypersensitivity reactions (6)."
Establishes localized skin inflammation, burrow formation, and rash as hallmark clinical manifestations of scabies infestation.
PMID:30755943 SUPPORT Human clinical
"The authors describe a clinical case of crusted scabies with pruritus and exuberant cutaneous lesions."
Reports cutaneous lesions in crusted scabies.
Recurrent bacterial skin infections FREQUENT HP:0005406 Human Phenotype Ontology (HP) Relation: this clinical feature is this phenotype This clinical feature is Recurrent bacterial skin infections (HP:0005406). HP:0005406 is a phenotype from the Human Phenotype Ontology.
Show evidence (2 references)
DOI:10.1371/journal.pntd.0009661 SUPPORT Other
"Scabies is a strong risk factor for superficial bacterial skin infection (impetigo), which can progress to severe bacterial infections, poststreptococcal glomerulonephritis, and possibly acute rheumatic fever and chronic kidney disease"
Identifies superficial bacterial skin infection (impetigo) and severe downstream bacterial and post-streptococcal complications as major clinical consequences of scabies.
DOI:10.1371/journal.pgph.0003706 SUPPORT Human clinical
"Scabies promotes bacterial SSTIs by causing breaches in the skin. These SSTIs range in severity from impetigo and other uncomplicated infections which can be generally treated in primary healthcare (PHC) settings"
Demonstrates that scabies-induced skin breaches promote bacterial skin and soft-tissue infections in endemic populations.
Integument 2
Pruritus VERY_FREQUENT HP:0000989 Human Phenotype Ontology (HP) Relation: this clinical feature is this phenotype This clinical feature is Pruritus (HP:0000989). HP:0000989 is a phenotype from the Human Phenotype Ontology.
Sequelae: Recurrent bacterial skin infections
Show evidence (2 references)
PMID:34925353 SUPPORT BACKGROUND Human clinical
"Infestation by the mite almost always leads to the development of localized skin inflammation, itching, and burrow formation; rash and itch possibly being an indicator of host immune response with features of both type I and type IV hypersensitivity reactions (6)."
Documents itching in almost all cases of ordinary scabies as a manifestation of the host immune response.
PMID:30755943 SUPPORT Human clinical
"The authors describe a clinical case of crusted scabies with pruritus and exuberant cutaneous lesions."
Reports pruritus in clinical scabies presentation.
Hyperkeratosis VERY_FREQUENT HP:0000962 Human Phenotype Ontology (HP) Relation: this clinical feature is this phenotype This clinical feature is Hyperkeratosis (HP:0000962). HP:0000962 is a phenotype from the Human Phenotype Ontology.
Show evidence (2 references)
PMID:30755943 SUPPORT Human clinical
"The immunophenotyping study was inconclusive and histological examination of the skin revealed marked hyperkeratosis with abundant arthropod parasites compatible with S. scabiei (Fig. 3)."
Histological confirmation of marked hyperkeratosis harboring abundant S. scabiei mites in crusted scabies.
PMID:34925353 SUPPORT BACKGROUND Human clinical
"IL-20 is also a proinflammatory cytokine produced by keratinocytes, monocytes, and endothelial cells and is associated with epidermal thickening, scales, and crusts in CS (19, 99)."
Documents epidermal thickening, scales, and hyperkeratotic crusts as characteristic features of crusted scabies.
💊

Medical Actions

2
Topical Permethrin
Action: PharmacotherapyNCI Thesaurus (NCIT) Relation: this treatment is this clinical intervention This treatment is Pharmacotherapy (NCIT:C15986). NCIT:C15986 is a clinical intervention from the NCI Thesaurus. NCIT:C15986
Agent: permethrin CHEBI:34911 Chemical Entities of Biological Interest (CHEBI) Relation: this treatment uses this therapeutic agent This treatment uses permethrin (CHEBI:34911). CHEBI:34911 is a therapeutic agent from Chemical Entities of Biological Interest.
Platform: Small molecule
First-line topical scabicidal pharmacotherapy (permethrin 5% cream) applied to the entire body surface to kill burrowing Sarcoptes scabiei mites in individual patients and household contacts.
Mechanism Target:
Mite infestation of the skin — Topical permethrin acts as a neurotoxic pyrethroid acaricide that eradicates burrowing S. scabiei mites in the stratum corneum.
Show evidence (1 reference)
DOI:10.1371/journal.pntd.0009661 SUPPORT Other
"Permethrin 5% is the preferred topical treatment."
Establishes 5% permethrin as the preferred topical acaricidal treatment for scabies.
Target Phenotypes: Pruritus HP:0000989 Human Phenotype Ontology (HP) Relation: this treatment targets this phenotype This treatment targets Pruritus (HP:0000989). HP:0000989 is a phenotype from the Human Phenotype Ontology. Skin rash HP:0000988 Human Phenotype Ontology (HP) Relation: this treatment targets this phenotype This treatment targets Skin rash (HP:0000988). HP:0000988 is a phenotype from the Human Phenotype Ontology.
Show evidence (2 references)
DOI:10.1371/journal.pntd.0009661 SUPPORT Other
"Permethrin 5% is the preferred topical treatment."
Identifies permethrin 5% cream as the preferred first-line topical therapy.
PMID:35298417 SUPPORT Other
"Mass treatment with permethrin cream or ivermectin can be given directly to patients."
Supports use of permethrin cream for direct patient and population treatment.
Oral Ivermectin
Action: PharmacotherapyNCI Thesaurus (NCIT) Relation: this treatment is this clinical intervention This treatment is Pharmacotherapy (NCIT:C15986). NCIT:C15986 is a clinical intervention from the NCI Thesaurus. NCIT:C15986
Agent: ivermectin CHEBI:6078 Chemical Entities of Biological Interest (CHEBI) Relation: this treatment uses this therapeutic agent This treatment uses ivermectin (CHEBI:6078). CHEBI:6078 is a therapeutic agent from Chemical Entities of Biological Interest.
Platform: Small molecule
Systemic antiparasitic pharmacotherapy administered as two oral doses of ivermectin (200 ug/kg given 7 to 14 days apart because ivermectin is not ovicidal) for individual case management, crusted scabies combination regimens, and community-wide mass drug administration (MDA) in endemic settings.
Mechanism Target:
Mite infestation of the skin — Oral ivermectin eradicates feeding S. scabiei mites in the epidermis; a second dose at 7 to 14 days eliminates newly hatched larvae.
Show evidence (1 reference)
DOI:10.1371/journal.pntd.0009661 SUPPORT Other
"The recommended regimen for MDA is 2 doses of oral ivermectin (200 μg/kg) given 7 to 14 days apart, using directly observed treatment wherever possible."
Documents the two-dose oral ivermectin regimen (200 ug/kg given 7 to 14 days apart) for scabies control.
Target Phenotypes: Pruritus HP:0000989 Human Phenotype Ontology (HP) Relation: this treatment targets this phenotype This treatment targets Pruritus (HP:0000989). HP:0000989 is a phenotype from the Human Phenotype Ontology. Skin rash HP:0000988 Human Phenotype Ontology (HP) Relation: this treatment targets this phenotype This treatment targets Skin rash (HP:0000988). HP:0000988 is a phenotype from the Human Phenotype Ontology.
Show evidence (2 references)
DOI:10.1371/journal.pntd.0009661 SUPPORT Other
"The recommended regimen for MDA is 2 doses of oral ivermectin (200 μg/kg) given 7 to 14 days apart, using directly observed treatment wherever possible."
Specifies the standard two-dose oral ivermectin regimen used in mass drug administration.
PMID:35298417 SUPPORT Other
"Mass treatment with permethrin cream or ivermectin can be given directly to patients."
Supports oral ivermectin for patient and mass treatment of scabies.
🔬

Diagnosis

3
2020 IACS Consensus Diagnostic Criteria
Standardized diagnostic framework developed by the International Alliance for the Control of Scabies (IACS) that stratifies diagnosis into three levels of certainty: Confirmed Scabies (direct visualization of the mite, eggs, or fecal pellets via microscopy, dermoscopy, or high-powered imaging), Clinical Scabies (scabies burrows or typical lesions in a classic distribution with itch and contact history), and Suspected Scabies.
Clinical Evaluation NCIT:C124351 NCI Thesaurus (NCIT)
Results: Positive clinical or suspected diagnosis based on burrows, typical lesion distribution, pruritus, and positive contact history, or confirmed diagnosis when mites/products are directly visualized.
Show evidence (1 reference)
DOI:10.1371/journal.pntd.0009661 SUPPORT Other
"the International Alliance for the Control of Scabies (IACS) categorize diagnosis into 1 of 3 levels of certainty: confirmed scabies (which requires specialized equipment to directly visualize the mite or its products), clinical scabies, and suspected scabies (which rely on clinical signs and..."
Describes the three-tier IACS consensus diagnostic framework for scabies.
Microscopic Examination of Skin Scrapings
Definitive parasitological diagnosis by light microscopic examination of skin scrapings taken from burrows or papules to directly identify Sarcoptes scabiei mites, ova, or fecal pellets (scybala), though sensitivity is low in ordinary scabies due to the low mite burden.
Microscopy NCIT:C16853 NCI Thesaurus (NCIT)
Results: Identification of whole S. scabiei mites, mite parts, eggs, or fecal pellets under light microscopy.
Show evidence (2 references)
DOI:10.1371/journal.pntd.0009661 SUPPORT Other
"Definitive diagnosis is made by microscopic examination of skin scrapings, which is insensitive and impractical in the field."
Establishes microscopic examination of skin scrapings as the definitive diagnostic test while noting its limited sensitivity in field settings.
PMID:34925353 SUPPORT PRIMARY RESULT Human clinical
"The cases of OS were confirmed by clinical observation and positive identification of mites and mite parts, collected from skin scrapings, under the microscope (1 mite or mite part/scraping)."
Illustrates diagnostic confirmation of ordinary scabies by microscopic identification of mites or mite parts in skin scrapings.
Dermoscopy
Non-invasive in vivo cutaneous surface microscopy used to visualize characteristic burrows and the pigmented anterior mite contour ("delta-wing jet with contrail" sign) within the stratum corneum.
Dermoscopy NCIT:C116478 NCI Thesaurus (NCIT)
Results: Direct visualization of S. scabiei mites and intracorneal burrows on dermoscopy.
Show evidence (1 reference)
PMID:30755943 SUPPORT Human clinical
"A diagnosis of crusted scabies can be confirmed by observing the mite through dermoscopy, or after skin scraping, an adhesive tape test or skin biopsy."
Supports confirmation of scabies diagnosis by direct visualization of the mite through dermoscopy.
📈

Progression

1
Incubation period
Incubation: 28-56 days (4-8 weeks) in primary infestation days
In primary human infestation, clinical skin inflammation and pruritus typically do not appear for 4 to 8 weeks (28-56 days) after initial infestation because live burrowing mites actively down-modulate early host innate inflammatory and adaptive immune responses.
Show evidence (1 reference)
PMID:23940705 SUPPORT BACKGROUND In vitro / ex vivo
"Hosts exhibit delayed inflammatory and adaptive immune responses to this parasite. In humans, clinical symptoms (skin inflammation) may not appear for 4 to 8 weeks after initial infestation. It is now clear that this delay is the result of the mite’s ability to modulate multiple aspects of the..."
Documents the 4-to-8-week latency of clinical skin inflammation in primary human infestation and attributes it to mite-mediated immunomodulation.
📊

Prevalence

1
High-burden endemic countries and crowded institutional settings (prisons, boarding schools, orphanages)
Point prevalence 32100.0–74000.0 per 100,000 >1 in 1,000
Point prevalence in high-burden countries and crowded institutional settings ranges from 32.1% to 74% (32,100 to 74,000 per 100,000 population).
Show evidence (1 reference)
PMID:35298417 SUPPORT Other
"The prevalence of scabies is high in certain countries ranging from 32.1% to 74%, especially in crowded conditions such as prisons, boarding schools, and orphanages."
Documents point prevalence ranging from 32.1% to 74% in high-burden countries and crowded institutional settings.
🦠

Infectious Agent

1
Sarcoptes scabiei
Ectoparasitic mite that burrows in the stratum corneum of human skin.
Sarcoptes scabiei NCBITaxon:52283 NCBI Taxonomy (NCBITaxon)
Show evidence (1 reference)
PMID:35298417 SUPPORT Other
"Scabies is a contagious parasitic skin disease caused by Sarcoptes scabiei infestation which can be transmitted through direct or indirect contact."
The abstract identifies S. scabiei infestation as the cause of scabies.
↔️

Transmission

1
Direct or indirect contact transmission
Transmitted through direct skin-to-skin contact or indirect fomite contact with infested individuals.
Show evidence (1 reference)
PMID:35298417 SUPPORT Other
"Scabies is a contagious parasitic skin disease caused by Sarcoptes scabiei infestation which can be transmitted through direct or indirect contact."
The abstract states transmission through direct or indirect contact.
📊

Related Datasets

2
Transcriptome analysis of the host immune responses to Sarcoptes scabiei geo:GSE178563
Scabies is a human skin disease due to the burrowing ectoparasite Sarcoptes scabiei resulting in intense itching and inflammation and manifesting as skin allergy. Little is known about the specific scabies molecules and genes involved in the host inflammatory and immunologic responses. We interrogated the transcriptome profiles of skin biopsies using next generation sequencing and a combined clustering and pathway mapping approach which will enable us in the identification of key signaling events in the host immune and inflammatory responses to S. scabiei infestation. With the comprehensive analysis of RNA-seq results, it has been found that the immune response of host inhibits S.
human BULK RNA SEQ n=8
PMID:34925353
Identified by GEO DataSets index search for Scabies (scripts/discover_datasets.py); accession and metadata verified against NCBI E-utilities on 2026-08-01. Title, sample count, and organism are GEO's own values.
Show evidence (1 reference)
PMID:34925353 SUPPORT PRIMARY RESULT Human clinical
"Here we aimed to interrogate the transcriptomic profiles of mite-infested human skin biopsies with clinical manifestations of ordinary scabies subjects ("OS"; n = 05) and subjects naive to scabies ("control"; n = 03) using RNASeq data analysis."
Primary publication generating the bulk RNA-seq dataset of human ordinary scabies and control skin biopsies.
Sarcoptes scabiei Mites Modulate Gene Expression In Human Skin Equivalents geo:GSE48459
The purpose of this study was to identify genes in keratinocytes and fibroblasts in human skin equivalents that changed expression in response to the burrowing of live scabies mites.
human MICROARRAY n=14
PMID:23940705
Identified by GEO DataSets index search for Scabies (scripts/discover_datasets.py); accession and metadata verified against NCBI E-utilities on 2026-08-01. Title, sample count, and organism are GEO's own values.
Show evidence (1 reference)
PMID:23940705 SUPPORT PRIMARY RESULT In vitro / ex vivo
"The purpose of this study was to identify genes in keratinocytes and fibroblasts in human skin equivalents (HSEs) that changed expression in response to the burrowing of live scabies mites."
Primary publication reporting the microarray dataset of human skin equivalents challenged with live burrowing S. scabiei mites.
{ }

Source YAML

click to show 
name: Scabies
creation_date: '2026-01-26T15:56:41Z'
category: Infectious Disease
description: >-
  Scabies is a contagious parasitic skin disease caused by infestation of the
  stratum corneum by the burrowing ectoparasitic mite Sarcoptes scabiei var.
  hominis. Mite burrowing and release of antigenic metabolites trigger host
  innate and adaptive immune responses involving epidermal keratinocytes,
  dermal fibroblasts, T lymphocytes, eosinophils, and mast cells, with features
  of both type I and delayed type IV hypersensitivity, manifesting clinically as
  intense pruritus and an inflammatory papulovesicular skin rash in ordinary
  scabies or severe hyperkeratotic crusted plaques in crusted scabies.
disease_term:
  term:
    id: MONDO:0004525
    label: scabies
  preferred_term: Scabies
parents:
- Parasitic infection
- Neglected tropical disease
has_subtypes:
- name: Ordinary Scabies
  display_name: Ordinary Scabies
  description: >-
    Classic clinical presentation in immunocompetent hosts characterized by a low
    mite burden and a protective CD4+ T-cell-dominated Th1 cell-mediated immune
    response, manifesting as burrows, erythematous papules, and intense pruritus.
  evidence:
  - reference: PMID:34925353
    reference_title: Transcriptome Analysis of Host Inflammatory Responses to the Ectoparasitic Mite Sarcoptes scabiei var. hominis.
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    quote_role: BACKGROUND
    snippet: "However, various studies have consistently shown that the immune response of the host to ordinary scabies is a Th1 cell-mediated protective type and to the crusted variety of the scabies is a non-protective Th2 allergic response (6, 17, 18)."
    explanation: Establishes that ordinary scabies elicits a protective Th1 cell-mediated host immune response distinct from crusted scabies.
  - reference: PMID:34925353
    reference_title: Transcriptome Analysis of Host Inflammatory Responses to the Ectoparasitic Mite Sarcoptes scabiei var. hominis.
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    quote_role: BACKGROUND
    snippet: "CD4+ T cells mostly dominate the infiltrates of skin biopsy lesions in ordinary scabies, with a 4:1 ratio of CD4+ to CD8+ T cells (12, 13)."
    explanation: Documents the CD4+ T-cell dominance (4:1 CD4+:CD8+ ratio) in skin lesions of ordinary scabies.
- name: Crusted Scabies
  display_name: Crusted (Norwegian) Scabies
  description: >-
    Severe, highly contagious form of scabies occurring predominantly in
    immunocompromised or elderly individuals, characterized by a non-protective
    Th2 allergic immune response (elevated IL-4, IL-5, IL-13, and IgE) with
    dermal CD8+ T-cell predominance, exuberant hyperkeratotic crusted lesions
    harboring abundant mites, and requirement for prolonged combination therapy.
  evidence:
  - reference: PMID:30755943
    reference_title: "An Itchy Problem: A Clinical Case of Crusted Scabies."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "A more severe form called crusted or Norwegian scabies may occur in immunosuppressed patients and the elderly. Crusted scabies mostly differs from normal scabies by the exuberance of its lesions, body distribution and high contagiousness, and requires different and more prolonged treatment."
    explanation: Defines crusted (Norwegian) scabies, its predilection for immunosuppressed and elderly hosts, exuberant lesions, high contagiousness, and distinct treatment needs.
  - reference: PMID:34925353
    reference_title: Transcriptome Analysis of Host Inflammatory Responses to the Ectoparasitic Mite Sarcoptes scabiei var. hominis.
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    quote_role: BACKGROUND
    snippet: "However, various studies have consistently shown that the immune response of the host to ordinary scabies is a Th1 cell-mediated protective type and to the crusted variety of the scabies is a non-protective Th2 allergic response (6, 17, 18). In addition, Crusted Scabies (CS) patients have shown increased production of Th2 cytokines IL-4, IL-5, and IL-13 and decreased secretion of the Th1 cytokine IFN-γ as compared to OS (19)."
    explanation: Characterizes the non-protective Th2 cytokine profile (increased IL-4, IL-5, and IL-13 with reduced IFN-gamma) in crusted scabies.
  - reference: PMID:34925353
    reference_title: Transcriptome Analysis of Host Inflammatory Responses to the Ectoparasitic Mite Sarcoptes scabiei var. hominis.
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    quote_role: BACKGROUND
    snippet: "In comparison, the skin inflammatory response in patients with crusted scabies predominantly comprises CD8+T cells (6, 12)."
    explanation: Documents CD8+ T-cell predominance in the cutaneous inflammatory infiltrate of crusted scabies.
classifications:
  harrisons_chapter:
  - classification_value: INFECTIOUS_DISEASES
    evidence:
    - reference: PMID:35298417
      reference_title: "Scabies: update on treatment and efforts for prevention and control in highly endemic settings."
      supports: SUPPORT
      evidence_source: OTHER
      snippet: "Scabies is a contagious parasitic skin disease caused by Sarcoptes scabiei infestation which can be transmitted through direct or indirect contact."
      explanation: Classifies scabies as a contagious parasitic infectious disease.
  - classification_value: DERMATOLOGY
    evidence:
    - reference: PMID:35298417
      reference_title: "Scabies: update on treatment and efforts for prevention and control in highly endemic settings."
      supports: SUPPORT
      evidence_source: OTHER
      snippet: "Scabies is a contagious parasitic skin disease caused by Sarcoptes scabiei infestation which can be transmitted through direct or indirect contact."
      explanation: Classifies scabies as a parasitic skin disease within dermatology.
prevalence:
- population: High-burden endemic countries and crowded institutional settings (prisons, boarding schools, orphanages)
  measure_type: POINT_PREVALENCE
  prevalence_class: ABOVE_1_IN_1000
  rate_low: 32100.0
  rate_high: 74000.0
  rate_denominator: POPULATION
  notes: >-
    Point prevalence in high-burden countries and crowded institutional settings
    ranges from 32.1% to 74% (32,100 to 74,000 per 100,000 population).
  evidence:
  - reference: PMID:35298417
    reference_title: "Scabies: update on treatment and efforts for prevention and control in highly endemic settings."
    supports: SUPPORT
    evidence_source: OTHER
    snippet: "The prevalence of scabies is high in certain countries ranging from 32.1% to 74%, especially in crowded conditions such as prisons, boarding schools, and orphanages."
    explanation: Documents point prevalence ranging from 32.1% to 74% in high-burden countries and crowded institutional settings.
progression:
- phase: Incubation period
  incubation_days: 28-56 days (4-8 weeks) in primary infestation
  notes: >-
    In primary human infestation, clinical skin inflammation and pruritus
    typically do not appear for 4 to 8 weeks (28-56 days) after initial
    infestation because live burrowing mites actively down-modulate early host
    innate inflammatory and adaptive immune responses.
  evidence:
  - reference: PMID:23940705
    reference_title: Sarcoptes scabiei mites modulate gene expression in human skin equivalents.
    supports: SUPPORT
    evidence_source: IN_VITRO
    quote_role: BACKGROUND
    snippet: "Hosts exhibit delayed inflammatory and adaptive immune responses to this parasite. In humans, clinical symptoms (skin inflammation) may not appear for 4 to 8 weeks after initial infestation. It is now clear that this delay is the result of the mite’s ability to modulate multiple aspects of the host’s inflammatory and immune responses."
    explanation: Documents the 4-to-8-week latency of clinical skin inflammation in primary human infestation and attributes it to mite-mediated immunomodulation.
infectious_agent:
- name: Sarcoptes scabiei
  infectious_agent_term:
    preferred_term: Sarcoptes scabiei
    term:
      id: NCBITaxon:52283
      label: Sarcoptes scabiei
  description: Ectoparasitic mite that burrows in the stratum corneum of human skin.
  evidence:
  - reference: PMID:35298417
    reference_title: "Scabies: update on treatment and efforts for prevention and control in highly endemic settings."
    supports: SUPPORT
    evidence_source: OTHER
    snippet: "Scabies is a contagious parasitic skin disease caused by Sarcoptes scabiei infestation which can be transmitted through direct or indirect contact."
    explanation: The abstract identifies S. scabiei infestation as the cause of scabies.
transmission:
- name: Direct or indirect contact transmission
  description: Transmitted through direct skin-to-skin contact or indirect fomite contact with infested individuals.
  evidence:
  - reference: PMID:35298417
    reference_title: "Scabies: update on treatment and efforts for prevention and control in highly endemic settings."
    supports: SUPPORT
    evidence_source: OTHER
    snippet: "Scabies is a contagious parasitic skin disease caused by Sarcoptes scabiei infestation which can be transmitted through direct or indirect contact."
    explanation: The abstract states transmission through direct or indirect contact.
pathophysiology:
- name: Mite infestation of the skin
  description: >-
    Sarcoptes scabiei var. hominis burrows into the stratum corneum of human
    epidermis and feeds on host epidermis and sera, releasing antigenic saliva,
    fecal pellets, and active metabolites that disrupt the epidermal barrier
    and initiate host cutaneous inflammatory and immune responses.
  biological_scale: TISSUE
  cell_types:
  - preferred_term: keratinocyte
    term:
      id: CL:0000312
      label: keratinocyte
  locations:
  - preferred_term: stratum corneum of epidermis
    term:
      id: UBERON:0002027
      label: stratum corneum of epidermis
  - preferred_term: skin epidermis
    term:
      id: UBERON:0001003
      label: skin epidermis
  evidence:
  - reference: PMID:34925353
    reference_title: Transcriptome Analysis of Host Inflammatory Responses to the Ectoparasitic Mite Sarcoptes scabiei var. hominis.
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    quote_role: BACKGROUND
    snippet: "S. scabiei var. hominis causes skin infestation in humans by forming burrows in the stratum corneum of the skin and feeding on host epidermis and sera. The release of active metabolites from the mite contribute to the intense itching and inflammation manifesting as a skin allergy and inflammatory responses (2). Potential sources of allergens include fecal material, mite bodies, mite saliva secreted at feeding, soluble proteins released after death in body fluids, and enzymes involved in molting and digestive processes (34)."
    explanation: Describes burrow formation in the stratum corneum, feeding on host epidermis and sera, and release of antigenic mite saliva, fecal material, and enzymes.
  - reference: PMID:30755943
    reference_title: "An Itchy Problem: A Clinical Case of Crusted Scabies."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "Scabies is an infestation of the skin by the mite Sarcoptes scabiei."
    explanation: Confirms cutaneous infestation by S. scabiei.
  downstream:
  - target: Keratinocyte and Fibroblast Cytokine and Keratinization Response
    causal_link_type: DIRECT
    description: Burrowing mites and secreted mite antigens directly stimulate resident epidermal keratinocytes and dermal fibroblasts.
    evidence:
    - reference: PMID:23940705
      reference_title: Sarcoptes scabiei mites modulate gene expression in human skin equivalents.
      supports: SUPPORT
      evidence_source: IN_VITRO
      quote_role: PRIMARY_RESULT
      snippet: "The purpose of this study was to identify genes in keratinocytes and fibroblasts in human skin equivalents (HSEs) that changed expression in response to the burrowing of live scabies mites."
      explanation: Demonstrates direct transcriptional modulation of epidermal keratinocytes and dermal fibroblasts in response to burrowing live S. scabiei mites.
  - target: Dermal Leukocyte and Granulocyte Infiltration
    causal_link_type: INDIRECT_KNOWN_INTERMEDIATES
    description: Mite products and keratinocyte/fibroblast chemokines recruit neutrophils, macrophages, T lymphocytes, eosinophils, and mast cells into the dermis.
    evidence:
    - reference: PMID:34925353
      reference_title: Transcriptome Analysis of Host Inflammatory Responses to the Ectoparasitic Mite Sarcoptes scabiei var. hominis.
      supports: SUPPORT
      evidence_source: HUMAN_CLINICAL
      quote_role: BACKGROUND
      snippet: "The initial immune response towards the mite and its products, by different hosts, consists of keratinocytes, neutrophils, Langerhans cells, and macrophages (7, 8), which initiate an inflammatory and immune reaction (9)."
      explanation: Links mite burrowing and antigen release to initiation of cutaneous leukocyte recruitment.
- name: Keratinocyte and Fibroblast Cytokine and Keratinization Response
  description: >-
    Epidermal keratinocytes and dermal fibroblasts respond to burrowing mites
    by upregulating innate proinflammatory cytokines and chemokines (including
    IL1A, IL1B, and CXCL8) alongside epidermal development and keratinization
    gene programs (including KRT6C, KRT9, SPRR2A, SPRR3, and LCE3A).
  biological_scale: CELLULAR
  cell_types:
  - preferred_term: keratinocyte
    term:
      id: CL:0000312
      label: keratinocyte
  - preferred_term: fibroblast
    term:
      id: CL:0000057
      label: fibroblast
  genes:
  - preferred_term: IL1A
    term:
      id: hgnc:5991
      label: IL1A
  - preferred_term: IL1B
    term:
      id: hgnc:5992
      label: IL1B
  - preferred_term: CXCL8
    term:
      id: hgnc:6025
      label: CXCL8
  biological_processes:
  - preferred_term: keratinization
    modifier: INCREASED
    term:
      id: GO:0031424
      label: keratinization
  - preferred_term: inflammatory response
    modifier: INCREASED
    term:
      id: GO:0006954
      label: inflammatory response
  locations:
  - preferred_term: skin epidermis
    term:
      id: UBERON:0001003
      label: skin epidermis
  - preferred_term: dermis
    term:
      id: UBERON:0002067
      label: dermis
  evidence:
  - reference: PMID:23940705
    reference_title: Sarcoptes scabiei mites modulate gene expression in human skin equivalents.
    supports: SUPPORT
    evidence_source: IN_VITRO
    quote_role: PRIMARY_RESULT
    snippet: "Genes for the expression of interleukin-1α (IL-1α) precursor, IL-1β, granulocyte/macrophage-colony stimulating factor (GM-CSF) precursor, and G-CSF precursor were up-regulated 2.8- to 7.4-fold, paralleling cytokine secretion profiles. A large number of genes involved in epithelium development and keratinization were also differentially expressed in response to live scabies mites."
    explanation: Demonstrates upregulation of IL1A, IL1B, and keratinization gene programs in human skin equivalents (keratinocytes and fibroblasts) challenged with live burrowing S. scabiei mites.
  - reference: PMID:34925353
    reference_title: Transcriptome Analysis of Host Inflammatory Responses to the Ectoparasitic Mite Sarcoptes scabiei var. hominis.
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    quote_role: PRIMARY_RESULT
    snippet: "Top upregulated genes displayed a role in inflammatory responses and innate immunity (DEFB4A, IL-19, CXCL8, CSF3, SERPINB4, S100A7A, HRNR), keratinization (KRT9, KRT6C, EGR4, SPRR3, LCE3A, SPRR2A, LCE3A), and a gene involved in desquamation processes in skin (SPINK9);"
    explanation: Human scabies skin biopsy RNA-seq confirms strong upregulation of CXCL8 and keratinization genes.
  - reference: PMID:34925353
    reference_title: Transcriptome Analysis of Host Inflammatory Responses to the Ectoparasitic Mite Sarcoptes scabiei var. hominis.
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    quote_role: PRIMARY_RESULT
    snippet: "As expected, the results showed that pathways associated with skin development, including keratinization, epidermis development, and keratinocyte differentiation, were highly upregulated in the diseased samples."
    explanation: Pathway enrichment analysis of human scabies lesions confirms upregulation of keratinization and keratinocyte differentiation.
  downstream:
  - target: Dermal Leukocyte and Granulocyte Infiltration
    causal_link_type: DIRECT
    description: Keratinocyte and fibroblast cytokines and chemokines (including IL-1alpha, IL-1beta, and CXCL8) recruit neutrophils, macrophages, T cells, and eosinophils to the dermis.
    evidence:
    - reference: PMID:34925353
      reference_title: Transcriptome Analysis of Host Inflammatory Responses to the Ectoparasitic Mite Sarcoptes scabiei var. hominis.
      supports: SUPPORT
      evidence_source: HUMAN_CLINICAL
      quote_role: BACKGROUND
      snippet: "The initial immune response towards the mite and its products, by different hosts, consists of keratinocytes, neutrophils, Langerhans cells, and macrophages (7, 8), which initiate an inflammatory and immune reaction (9). Granulocytes are engaged in boosting the immunity of the host against a variety of parasites by initiating immunomodulation and producing cytokines and chemokines, which direct the immune response."
      explanation: Supports cytokine- and chemokine-directed recruitment of immune cells in scabies skin lesions.
  - target: JAK-STAT Signaling Pathway Activation
    causal_link_type: DIRECT
    description: Secreted epidermal and dermal cytokines engage cell-surface receptors to activate intracellular JAK-STAT signaling cascades in lesional skin.
    evidence:
    - reference: PMID:34925353
      reference_title: Transcriptome Analysis of Host Inflammatory Responses to the Ectoparasitic Mite Sarcoptes scabiei var. hominis.
      supports: SUPPORT
      evidence_source: HUMAN_CLINICAL
      quote_role: PRIMARY_RESULT
      snippet: "The clustering patterns showed various differentially expressed genes including inflammatory responses and innate immunity genes (DEFB4A, IL-19, CXCL8, CSF3, SERPINB4, S100A7A, HRNR) and notably upregulation of the JAK-STAT pathway in scabies-infested samples."
      explanation: Links innate cytokine induction to upregulation of the JAK-STAT pathway in scabies-infested human skin.
  - target: Hyperkeratosis
    causal_link_type: INDIRECT_KNOWN_INTERMEDIATES
    description: Sustained upregulation of epidermal keratinization programs and keratinocyte-derived IL-20 signaling drives epidermal thickening, scaling, and hyperkeratotic crust formation in crusted scabies.
    evidence:
    - reference: PMID:34925353
      reference_title: Transcriptome Analysis of Host Inflammatory Responses to the Ectoparasitic Mite Sarcoptes scabiei var. hominis.
      supports: SUPPORT
      evidence_source: HUMAN_CLINICAL
      quote_role: BACKGROUND
      snippet: "IL-20 is also a proinflammatory cytokine produced by keratinocytes, monocytes, and endothelial cells and is associated with epidermal thickening, scales, and crusts in CS (19, 99)."
      explanation: Links keratinocyte cytokine production and epidermal proliferation to hyperkeratotic scales and crusts in crusted scabies.
- name: Dermal Leukocyte and Granulocyte Infiltration
  description: >-
    Recruitment and accumulation of T lymphocytes, macrophages, neutrophils,
    eosinophils, and mast cells in the dermis. In ordinary scabies, CD4+ T
    lymphocytes predominate in a 4:1 ratio over CD8+ T cells as part of a
    protective Th1 cell-mediated response, whereas crusted scabies exhibits
    dermal CD8+ T-cell predominance alongside heavy eosinophil, lymphocyte, and
    macrophage infiltration.
  biological_scale: TISSUE
  cell_types:
  - preferred_term: T cell
    term:
      id: CL:0000084
      label: T cell
  - preferred_term: macrophage
    term:
      id: CL:0000235
      label: macrophage
  - preferred_term: eosinophil
    term:
      id: CL:0000771
      label: eosinophil
  - preferred_term: mast cell
    term:
      id: CL:0000097
      label: mast cell
  - preferred_term: neutrophil
    term:
      id: CL:0000775
      label: neutrophil
  biological_processes:
  - preferred_term: leukocyte chemotaxis
    modifier: INCREASED
    term:
      id: GO:0030595
      label: leukocyte chemotaxis
  - preferred_term: immune response
    modifier: INCREASED
    term:
      id: GO:0006955
      label: immune response
  locations:
  - preferred_term: dermis
    term:
      id: UBERON:0002067
      label: dermis
  evidence:
  - reference: PMID:34925353
    reference_title: Transcriptome Analysis of Host Inflammatory Responses to the Ectoparasitic Mite Sarcoptes scabiei var. hominis.
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    quote_role: BACKGROUND
    snippet: "Upon recruitment to infection site/draining lymph nodes, eosinophils, mast cells, and basophils produce IL-4 and /or IL-13 (10). In a study reported by Walton et al. in 2008, skin biopsies taken from scabies patients having crusted lesions showed large numbers of lymphocytes, monocytes, macrophages, and eosinophils in the dermis, with increased levels of IgE in the blood samples."
    explanation: Documents recruitment of eosinophils, mast cells, lymphocytes, monocytes, and macrophages into the dermis of scabies lesions.
  - reference: PMID:34925353
    reference_title: Transcriptome Analysis of Host Inflammatory Responses to the Ectoparasitic Mite Sarcoptes scabiei var. hominis.
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    quote_role: BACKGROUND
    snippet: "The immune response to S. scabiei consistently shows increased levels of CD4+ or CD8+ T cells. CD4+ T cells mostly dominate the infiltrates of skin biopsy lesions in ordinary scabies, with a 4:1 ratio of CD4+ to CD8+ T cells (12, 13)."
    explanation: Demonstrates dermal T-cell infiltration with CD4+ T-cell dominance in ordinary scabies and CD8+ T-cell involvement.
  downstream:
  - target: Type 2 Cytokine and IL-31 Pruritogenic Signaling
    causal_link_type: DIRECT
    description: Infiltrating T cells, eosinophils, and mast cells secrete type 2 and pruritogenic cytokines including IL-4, IL-13, and IL-31.
    evidence:
    - reference: PMID:34925353
      reference_title: Transcriptome Analysis of Host Inflammatory Responses to the Ectoparasitic Mite Sarcoptes scabiei var. hominis.
      supports: SUPPORT
      evidence_source: HUMAN_CLINICAL
      quote_role: BACKGROUND
      snippet: "Upon recruitment to infection site/draining lymph nodes, eosinophils, mast cells, and basophils produce IL-4 and /or IL-13 (10)."
      explanation: Directly links recruited eosinophils and mast cells to IL-4 and IL-13 production in scabies lesions.
  - target: Skin rash
    causal_link_type: DIRECT
    description: Combined type I and delayed type IV dermal cellular infiltration produces erythematous papules and inflammatory skin lesions.
    evidence:
    - reference: PMID:34925353
      reference_title: Transcriptome Analysis of Host Inflammatory Responses to the Ectoparasitic Mite Sarcoptes scabiei var. hominis.
      supports: SUPPORT
      evidence_source: HUMAN_CLINICAL
      quote_role: BACKGROUND
      snippet: "Infestation by the mite almost always leads to the development of localized skin inflammation, itching, and burrow formation; rash and itch possibly being an indicator of host immune response with features of both type I and type IV hypersensitivity reactions (6)."
      explanation: Connects the combined type I and type IV hypersensitivity immune response to localized skin inflammation and rash.
- name: JAK-STAT Signaling Pathway Activation
  description: >-
    Transcriptional and functional upregulation of the intracellular JAK-STAT
    signaling cascade in scabies-infested skin, promoting macrophage and
    neutrophil activation, B- and T-lymphocyte differentiation, and
    amplification of cytokine-mediated cutaneous inflammation.
  biological_scale: MOLECULAR
  biological_processes:
  - preferred_term: cell surface receptor signaling pathway via JAK-STAT
    modifier: INCREASED
    term:
      id: GO:0007259
      label: cell surface receptor signaling pathway via JAK-STAT
  locations:
  - preferred_term: skin of body
    term:
      id: UBERON:0002097
      label: skin of body
  evidence:
  - reference: PMID:34925353
    reference_title: Transcriptome Analysis of Host Inflammatory Responses to the Ectoparasitic Mite Sarcoptes scabiei var. hominis.
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    quote_role: PRIMARY_RESULT
    snippet: "The clustering patterns showed various differentially expressed genes including inflammatory responses and innate immunity genes (DEFB4A, IL-19, CXCL8, CSF3, SERPINB4, S100A7A, HRNR) and notably upregulation of the JAK-STAT pathway in scabies-infested samples."
    explanation: Bulk RNA-seq of human scabies skin biopsies identifies prominent upregulation of the JAK-STAT signaling pathway.
  - reference: PMID:34925353
    reference_title: Transcriptome Analysis of Host Inflammatory Responses to the Ectoparasitic Mite Sarcoptes scabiei var. hominis.
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    quote_role: BACKGROUND
    snippet: "Differentially expressed genes that were enhanced in OS included immune-related signaling pathways and JAK-STAT pathways. Their impacts include activation of macrophages and neutrophils, host inflammatory responses, and the differentiation of B and T cells, which control the wound repair (67)."
    explanation: Details the functional consequences of JAK-STAT pathway activation in ordinary scabies skin lesions.
  downstream:
  - target: Type 2 Cytokine and IL-31 Pruritogenic Signaling
    causal_link_type: DIRECT
    description: JAK-STAT pathway activation transduces and amplifies IL-4, IL-13, and IL-31 cytokine signaling in lesional skin.
    evidence:
    - reference: PMID:34925353
      reference_title: Transcriptome Analysis of Host Inflammatory Responses to the Ectoparasitic Mite Sarcoptes scabiei var. hominis.
      supports: SUPPORT
      evidence_source: HUMAN_CLINICAL
      quote_role: PRIMARY_RESULT
      snippet: "Marked enrichment of immune response pathways (JAK-STAT signaling, IL-4 and IL-13 pathway, and Toll receptor cascade), chemokine ligands and receptors (CCL17, CCL18, CCL3L1, CCL3L3, CCR7), and cytokines (IL-13 and IL-20) were observed."
      explanation: Demonstrates co-enrichment of JAK-STAT signaling and the IL-4/IL-13 cytokine pathway in scabies lesions.
- name: Type 2 Cytokine and IL-31 Pruritogenic Signaling
  description: >-
    Upregulation of type 2 cytokines (IL4, IL13) and the pruritogenic cytokine
    IL31, alongside Th2-associated chemokines (CCL17, CCL18), in mite-infested
    skin. IL-4 sensitizes pruriceptors to histamine and IL-31 signals to induce
    severe pruritus, with expression levels correlating directly with clinical
    itch severity scores.
  biological_scale: MOLECULAR
  cell_types:
  - preferred_term: T cell
    term:
      id: CL:0000084
      label: T cell
  - preferred_term: eosinophil
    term:
      id: CL:0000771
      label: eosinophil
  - preferred_term: mast cell
    term:
      id: CL:0000097
      label: mast cell
  genes:
  - preferred_term: IL4
    term:
      id: hgnc:6014
      label: IL4
  - preferred_term: IL13
    term:
      id: hgnc:5973
      label: IL13
  - preferred_term: IL31
    term:
      id: hgnc:19372
      label: IL31
  biological_processes:
  - preferred_term: type I hypersensitivity
    modifier: INCREASED
    term:
      id: GO:0016068
      label: type I hypersensitivity
  locations:
  - preferred_term: skin of body
    term:
      id: UBERON:0002097
      label: skin of body
  evidence:
  - reference: PMID:34925353
    reference_title: Transcriptome Analysis of Host Inflammatory Responses to the Ectoparasitic Mite Sarcoptes scabiei var. hominis.
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    quote_role: PRIMARY_RESULT
    snippet: "DEGs in scabies mite-infested skin included those encoding certain chemokines (C-C motif) ligands CCL2, CCL17, and CCL 18, (C-X-C motif) ligand CXCL1, IL-17A, IL-17F, IL-23, IL-31 with FC greater than two for most of the genes. IL-4, CCL7, CCL20, IL-19, IL-20, IL-36A were also prominent DEGs with high FCs that were significantly correlated with the itch severity scores."
    explanation: Demonstrates significant upregulation of IL31 and IL4 in human scabies lesions and correlation of IL4 with clinical itch severity scores.
  - reference: PMID:34925353
    reference_title: Transcriptome Analysis of Host Inflammatory Responses to the Ectoparasitic Mite Sarcoptes scabiei var. hominis.
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    quote_role: PRIMARY_RESULT
    snippet: "Marked enrichment of immune response pathways (JAK-STAT signaling, IL-4 and IL-13 pathway, and Toll receptor cascade), chemokine ligands and receptors (CCL17, CCL18, CCL3L1, CCL3L3, CCR7), and cytokines (IL-13 and IL-20) were observed."
    explanation: Confirms enrichment of the IL-4 and IL-13 pathway and upregulation of IL13 in human scabies lesions.
  - reference: PMID:34925353
    reference_title: Transcriptome Analysis of Host Inflammatory Responses to the Ectoparasitic Mite Sarcoptes scabiei var. hominis.
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    quote_role: BACKGROUND
    snippet: "IL-4 and IL-31 were also significantly high in scabies mite-infested skin. IL-4 is reported to increase the itching even in low dose of histamine (91), and IL-31 is known to be involved in causing itching by signal activation of IL-13 receptors, but the mechanism involved is still unclear (92)."
    explanation: Explains how elevated IL-4 and IL-31 in scabies-infested skin drive itching through histamine sensitization and receptor signaling.
  downstream:
  - target: Pruritus
    causal_link_type: DIRECT
    description: Elevated IL-4, IL-13, and IL-31 in lesional skin directly stimulate and sensitize cutaneous sensory nerve fibers to produce intense pruritus.
    evidence:
    - reference: PMID:34925353
      reference_title: Transcriptome Analysis of Host Inflammatory Responses to the Ectoparasitic Mite Sarcoptes scabiei var. hominis.
      supports: SUPPORT
      evidence_source: HUMAN_CLINICAL
      quote_role: BACKGROUND
      snippet: "IL-4 and IL-31 were also significantly high in scabies mite-infested skin. IL-4 is reported to increase the itching even in low dose of histamine (91), and IL-31 is known to be involved in causing itching by signal activation of IL-13 receptors, but the mechanism involved is still unclear (92)."
      explanation: Directly links elevated cutaneous IL-4 and IL-31 to pruritus in scabies.
phenotypes:
- name: Pruritus
  category: Dermatologic
  diagnostic: true
  frequency: VERY_FREQUENT
  description: >-
    Intense generalized or localized itching, characteristically worse at night,
    resulting from host type I and type IV hypersensitivity responses and IL-4/IL-31
    pruritogenic signaling in response to burrowing mites and their antigens.
  phenotype_term:
    preferred_term: Pruritus
    term:
      id: HP:0000989
      label: Pruritus
  evidence:
  - reference: PMID:34925353
    reference_title: Transcriptome Analysis of Host Inflammatory Responses to the Ectoparasitic Mite Sarcoptes scabiei var. hominis.
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    quote_role: BACKGROUND
    snippet: "Infestation by the mite almost always leads to the development of localized skin inflammation, itching, and burrow formation; rash and itch possibly being an indicator of host immune response with features of both type I and type IV hypersensitivity reactions (6)."
    explanation: Documents itching in almost all cases of ordinary scabies as a manifestation of the host immune response.
  - reference: PMID:30755943
    reference_title: "An Itchy Problem: A Clinical Case of Crusted Scabies."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "The authors describe a clinical case of crusted scabies with pruritus and exuberant cutaneous lesions."
    explanation: Reports pruritus in clinical scabies presentation.
  sequelae:
  - target: Recurrent bacterial skin infections
    causal_link_type: DIRECT
    description: Scratching induced by intense pruritus breaches the epidermal barrier, facilitating secondary bacterial skin and soft-tissue infections.
    evidence:
    - reference: DOI:10.1371/journal.pgph.0003706
      reference_title: Costs of primary healthcare presentations and hospital admissions for scabies and related skin infections in Fiji, 2018–2019
      supports: SUPPORT
      evidence_source: HUMAN_CLINICAL
      snippet: "Scabies promotes bacterial SSTIs by causing breaches in the skin. These SSTIs range in severity from impetigo and other uncomplicated infections which can be generally treated in primary healthcare (PHC) settings"
      explanation: Documents that scabies-induced skin breaches promote secondary bacterial skin and soft-tissue infections such as impetigo.
- name: Skin rash
  category: Dermatologic
  diagnostic: true
  frequency: VERY_FREQUENT
  description: >-
    Inflammatory cutaneous eruption with burrows, erythematous papules, and
    excoriations in ordinary scabies, or exuberant psoriasiform plaques in
    crusted scabies.
  phenotype_term:
    preferred_term: Skin rash
    term:
      id: HP:0000988
      label: Skin rash
  evidence:
  - reference: PMID:34925353
    reference_title: Transcriptome Analysis of Host Inflammatory Responses to the Ectoparasitic Mite Sarcoptes scabiei var. hominis.
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    quote_role: BACKGROUND
    snippet: "Infestation by the mite almost always leads to the development of localized skin inflammation, itching, and burrow formation; rash and itch possibly being an indicator of host immune response with features of both type I and type IV hypersensitivity reactions (6)."
    explanation: Establishes localized skin inflammation, burrow formation, and rash as hallmark clinical manifestations of scabies infestation.
  - reference: PMID:30755943
    reference_title: "An Itchy Problem: A Clinical Case of Crusted Scabies."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "The authors describe a clinical case of crusted scabies with pruritus and exuberant cutaneous lesions."
    explanation: Reports cutaneous lesions in crusted scabies.
  sequelae:
  - target: Recurrent bacterial skin infections
    causal_link_type: DIRECT
    description: Epidermal burrows and inflammatory skin lesions disrupt skin barrier integrity and predispose to bacterial superinfection (impetigo).
    evidence:
    - reference: DOI:10.1371/journal.pntd.0009661
      reference_title: A framework for scabies control
      supports: SUPPORT
      evidence_source: OTHER
      snippet: "Scabies is a strong risk factor for superficial bacterial skin infection (impetigo), which can progress to severe bacterial infections, poststreptococcal glomerulonephritis, and possibly acute rheumatic fever and chronic kidney disease"
      explanation: Establishes scabies lesions as a major risk factor for superficial bacterial skin infection (impetigo) and downstream invasive or post-streptococcal sequelae.
- name: Hyperkeratosis
  subtype: Crusted Scabies
  category: Dermatologic
  frequency: VERY_FREQUENT
  description: >-
    Marked epidermal thickening with exuberant, scaly, hyperkeratotic crusted
    plaques teeming with mites, characteristic of crusted (Norwegian) scabies.
  phenotype_term:
    preferred_term: Hyperkeratosis
    term:
      id: HP:0000962
      label: Hyperkeratosis
  evidence:
  - reference: PMID:30755943
    reference_title: "An Itchy Problem: A Clinical Case of Crusted Scabies."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "The immunophenotyping study was inconclusive and histological examination of the skin revealed marked hyperkeratosis with abundant arthropod parasites compatible with S. scabiei (Fig. 3)."
    explanation: Histological confirmation of marked hyperkeratosis harboring abundant S. scabiei mites in crusted scabies.
  - reference: PMID:34925353
    reference_title: Transcriptome Analysis of Host Inflammatory Responses to the Ectoparasitic Mite Sarcoptes scabiei var. hominis.
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    quote_role: BACKGROUND
    snippet: "IL-20 is also a proinflammatory cytokine produced by keratinocytes, monocytes, and endothelial cells and is associated with epidermal thickening, scales, and crusts in CS (19, 99)."
    explanation: Documents epidermal thickening, scales, and hyperkeratotic crusts as characteristic features of crusted scabies.
- name: Recurrent bacterial skin infections
  category: Dermatologic
  frequency: FREQUENT
  description: >-
    Secondary bacterial skin and soft-tissue infections, most commonly
    superficial impetigo caused by Streptococcus pyogenes or Staphylococcus
    aureus entering through mite burrows and excoriations, which can progress
    to severe soft-tissue infection, invasive sepsis, or post-streptococcal
    glomerulonephritis in endemic settings.
  phenotype_term:
    preferred_term: Recurrent bacterial skin infections
    term:
      id: HP:0005406
      label: Recurrent bacterial skin infections
  evidence:
  - reference: DOI:10.1371/journal.pntd.0009661
    reference_title: A framework for scabies control
    supports: SUPPORT
    evidence_source: OTHER
    snippet: "Scabies is a strong risk factor for superficial bacterial skin infection (impetigo), which can progress to severe bacterial infections, poststreptococcal glomerulonephritis, and possibly acute rheumatic fever and chronic kidney disease"
    explanation: Identifies superficial bacterial skin infection (impetigo) and severe downstream bacterial and post-streptococcal complications as major clinical consequences of scabies.
  - reference: DOI:10.1371/journal.pgph.0003706
    reference_title: Costs of primary healthcare presentations and hospital admissions for scabies and related skin infections in Fiji, 2018–2019
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "Scabies promotes bacterial SSTIs by causing breaches in the skin. These SSTIs range in severity from impetigo and other uncomplicated infections which can be generally treated in primary healthcare (PHC) settings"
    explanation: Demonstrates that scabies-induced skin breaches promote bacterial skin and soft-tissue infections in endemic populations.
diagnosis:
- name: 2020 IACS Consensus Diagnostic Criteria
  diagnosis_term:
    preferred_term: Clinical Evaluation
    term:
      id: NCIT:C124351
      label: Clinical Evaluation
  description: >-
    Standardized diagnostic framework developed by the International Alliance for
    the Control of Scabies (IACS) that stratifies diagnosis into three levels of
    certainty: Confirmed Scabies (direct visualization of the mite, eggs, or
    fecal pellets via microscopy, dermoscopy, or high-powered imaging), Clinical
    Scabies (scabies burrows or typical lesions in a classic distribution with
    itch and contact history), and Suspected Scabies.
  results: >-
    Positive clinical or suspected diagnosis based on burrows, typical lesion
    distribution, pruritus, and positive contact history, or confirmed diagnosis
    when mites/products are directly visualized.
  evidence:
  - reference: DOI:10.1371/journal.pntd.0009661
    reference_title: A framework for scabies control
    supports: SUPPORT
    evidence_source: OTHER
    snippet: "the International Alliance for the Control of Scabies (IACS) categorize diagnosis into 1 of 3 levels of certainty: confirmed scabies (which requires specialized equipment to directly visualize the mite or its products), clinical scabies, and suspected scabies (which rely on clinical signs and history features)"
    explanation: Describes the three-tier IACS consensus diagnostic framework for scabies.
- name: Microscopic Examination of Skin Scrapings
  diagnosis_term:
    preferred_term: Microscopy
    term:
      id: NCIT:C16853
      label: Microscopy
  description: >-
    Definitive parasitological diagnosis by light microscopic examination of
    skin scrapings taken from burrows or papules to directly identify Sarcoptes
    scabiei mites, ova, or fecal pellets (scybala), though sensitivity is low in
    ordinary scabies due to the low mite burden.
  results: >-
    Identification of whole S. scabiei mites, mite parts, eggs, or fecal pellets
    under light microscopy.
  evidence:
  - reference: DOI:10.1371/journal.pntd.0009661
    reference_title: A framework for scabies control
    supports: SUPPORT
    evidence_source: OTHER
    snippet: "Definitive diagnosis is made by microscopic examination of skin scrapings, which is insensitive and impractical in the field."
    explanation: Establishes microscopic examination of skin scrapings as the definitive diagnostic test while noting its limited sensitivity in field settings.
  - reference: PMID:34925353
    reference_title: Transcriptome Analysis of Host Inflammatory Responses to the Ectoparasitic Mite Sarcoptes scabiei var. hominis.
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    quote_role: PRIMARY_RESULT
    snippet: "The cases of OS were confirmed by clinical observation and positive identification of mites and mite parts, collected from skin scrapings, under the microscope (1 mite or mite part/scraping)."
    explanation: Illustrates diagnostic confirmation of ordinary scabies by microscopic identification of mites or mite parts in skin scrapings.
- name: Dermoscopy
  diagnosis_term:
    preferred_term: Dermoscopy
    term:
      id: NCIT:C116478
      label: Dermoscopy
  description: >-
    Non-invasive in vivo cutaneous surface microscopy used to visualize
    characteristic burrows and the pigmented anterior mite contour ("delta-wing
    jet with contrail" sign) within the stratum corneum.
  results: >-
    Direct visualization of S. scabiei mites and intracorneal burrows on
    dermoscopy.
  evidence:
  - reference: PMID:30755943
    reference_title: "An Itchy Problem: A Clinical Case of Crusted Scabies."
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "A diagnosis of crusted scabies can be confirmed by observing the mite through dermoscopy, or after skin scraping, an adhesive tape test or skin biopsy."
    explanation: Supports confirmation of scabies diagnosis by direct visualization of the mite through dermoscopy.
treatments:
- name: Topical Permethrin
  description: >-
    First-line topical scabicidal pharmacotherapy (permethrin 5% cream) applied
    to the entire body surface to kill burrowing Sarcoptes scabiei mites in
    individual patients and household contacts.
  therapeutic_modality: SMALL_MOLECULE
  treatment_term:
    preferred_term: Pharmacotherapy
    term:
      id: NCIT:C15986
      label: Pharmacotherapy
    therapeutic_agent:
    - preferred_term: permethrin
      term:
        id: CHEBI:34911
        label: permethrin
  target_mechanisms:
  - target: Mite infestation of the skin
    description: Topical permethrin acts as a neurotoxic pyrethroid acaricide that eradicates burrowing S. scabiei mites in the stratum corneum.
    evidence:
    - reference: DOI:10.1371/journal.pntd.0009661
      reference_title: A framework for scabies control
      supports: SUPPORT
      evidence_source: OTHER
      snippet: "Permethrin 5% is the preferred topical treatment."
      explanation: Establishes 5% permethrin as the preferred topical acaricidal treatment for scabies.
  target_phenotypes:
  - preferred_term: Pruritus
    term:
      id: HP:0000989
      label: Pruritus
  - preferred_term: Skin rash
    term:
      id: HP:0000988
      label: Skin rash
  evidence:
  - reference: DOI:10.1371/journal.pntd.0009661
    reference_title: A framework for scabies control
    supports: SUPPORT
    evidence_source: OTHER
    snippet: "Permethrin 5% is the preferred topical treatment."
    explanation: Identifies permethrin 5% cream as the preferred first-line topical therapy.
  - reference: PMID:35298417
    reference_title: "Scabies: update on treatment and efforts for prevention and control in highly endemic settings."
    supports: SUPPORT
    evidence_source: OTHER
    snippet: "Mass treatment with permethrin cream or ivermectin can be given directly to patients."
    explanation: Supports use of permethrin cream for direct patient and population treatment.
- name: Oral Ivermectin
  description: >-
    Systemic antiparasitic pharmacotherapy administered as two oral doses of
    ivermectin (200 ug/kg given 7 to 14 days apart because ivermectin is not
    ovicidal) for individual case management, crusted scabies combination
    regimens, and community-wide mass drug administration (MDA) in endemic
    settings.
  therapeutic_modality: SMALL_MOLECULE
  treatment_term:
    preferred_term: Pharmacotherapy
    term:
      id: NCIT:C15986
      label: Pharmacotherapy
    therapeutic_agent:
    - preferred_term: ivermectin
      term:
        id: CHEBI:6078
        label: ivermectin
  target_mechanisms:
  - target: Mite infestation of the skin
    description: Oral ivermectin eradicates feeding S. scabiei mites in the epidermis; a second dose at 7 to 14 days eliminates newly hatched larvae.
    evidence:
    - reference: DOI:10.1371/journal.pntd.0009661
      reference_title: A framework for scabies control
      supports: SUPPORT
      evidence_source: OTHER
      snippet: "The recommended regimen for MDA is 2 doses of oral ivermectin (200 μg/kg) given 7 to 14 days apart, using directly observed treatment wherever possible."
      explanation: Documents the two-dose oral ivermectin regimen (200 ug/kg given 7 to 14 days apart) for scabies control.
  target_phenotypes:
  - preferred_term: Pruritus
    term:
      id: HP:0000989
      label: Pruritus
  - preferred_term: Skin rash
    term:
      id: HP:0000988
      label: Skin rash
  evidence:
  - reference: DOI:10.1371/journal.pntd.0009661
    reference_title: A framework for scabies control
    supports: SUPPORT
    evidence_source: OTHER
    snippet: "The recommended regimen for MDA is 2 doses of oral ivermectin (200 μg/kg) given 7 to 14 days apart, using directly observed treatment wherever possible."
    explanation: Specifies the standard two-dose oral ivermectin regimen used in mass drug administration.
  - reference: PMID:35298417
    reference_title: "Scabies: update on treatment and efforts for prevention and control in highly endemic settings."
    supports: SUPPORT
    evidence_source: OTHER
    snippet: "Mass treatment with permethrin cream or ivermectin can be given directly to patients."
    explanation: Supports oral ivermectin for patient and mass treatment of scabies.
references:
- reference: DOI:10.1007/s00436-024-08173-6
  title: 'Scabies: Immunopathogenesis and pathological changes'
  found_in:
  - Scabies-deep-research-falcon.md
  findings: []
- reference: DOI:10.1007/s00436-024-08298-8
  title: 'Scabies vaccines: where we stand and challenges ahead'
  found_in:
  - Scabies-deep-research-falcon.md
  findings: []
- reference: DOI:10.1101/2024.11.25.24317899
  title: 'Impact of Scabies on Quality of Life and Recent Advances in Management: A Systematic Review'
  found_in:
  - Scabies-deep-research-falcon.md
  findings:
  - statement: Scabies are a highly transmittable disease of the skin.
    supporting_text: Scabies are a highly transmittable disease of the skin.
    evidence:
    - reference: DOI:10.1101/2024.11.25.24317899
      reference_title: 'Impact of Scabies on Quality of Life and Recent Advances in Management: A Systematic Review'
      supports: SUPPORT
      evidence_source: OTHER
      snippet: Scabies are a highly transmittable disease of the skin.
      explanation: Deep research cited this publication as relevant literature for Scabies.
- reference: DOI:10.1111/bjd.19170
  title: 'Estimating the global burden of scabies: what else do we need?*'
  found_in:
  - Scabies-deep-research-falcon.md
  findings: []
- reference: DOI:10.1111/jdv.19167
  title: Prevalence of scabies worldwide—An updated systematic literature review in 2022
  found_in:
  - Scabies-deep-research-falcon.md
  findings:
  - statement: Scabies is a World Health Organization‐defined neglected tropical disease, with continuously rising incidence worldwide in recent years.
    supporting_text: Scabies is a World Health Organization‐defined neglected tropical disease, with continuously rising incidence worldwide in recent years.
    evidence:
    - reference: DOI:10.1111/jdv.19167
      reference_title: Prevalence of scabies worldwide—An updated systematic literature review in 2022
      supports: SUPPORT
      evidence_source: OTHER
      snippet: Scabies is a World Health Organization‐defined neglected tropical disease, with continuously rising incidence worldwide in recent years.
      explanation: Deep research cited this publication as relevant literature for Scabies.
- reference: DOI:10.1111/jdv.19288
  title: Detection of a knockdown mutation in the voltage‐sensitive sodium channel associated with permethrin tolerance in <i>Sarcoptes scabiei</i> var. <i>hominis</i> mites
  found_in:
  - Scabies-deep-research-falcon.md
  findings:
  - statement: Increasing evidence has sparked a debate on the loss of sensitivity of scabies mites to conventional permethrin therapy.
    supporting_text: Increasing evidence has sparked a debate on the loss of sensitivity of scabies mites to conventional permethrin therapy.
    evidence:
    - reference: DOI:10.1111/jdv.19288
      reference_title: Detection of a knockdown mutation in the voltage‐sensitive sodium channel associated with permethrin tolerance in <i>Sarcoptes scabiei</i> var. <i>hominis</i> mites
      supports: SUPPORT
      evidence_source: OTHER
      snippet: Increasing evidence has sparked a debate on the loss of sensitivity of scabies mites to conventional permethrin therapy.
      explanation: Deep research cited this publication as relevant literature for Scabies.
- reference: DOI:10.1371/journal.pgph.0003706
  title: Costs of primary healthcare presentations and hospital admissions for scabies and related skin infections in Fiji, 2018–2019
  found_in:
  - Scabies-deep-research-falcon.md
  findings:
  - statement: Scabies and related bacterial skin and soft tissue infections (SSTIs) are highly prevalent in many tropical, low- and middle-income settings.
    supporting_text: Scabies and related bacterial skin and soft tissue infections (SSTIs) are highly prevalent in many tropical, low- and middle-income settings.
    evidence:
    - reference: DOI:10.1371/journal.pgph.0003706
      reference_title: Costs of primary healthcare presentations and hospital admissions for scabies and related skin infections in Fiji, 2018–2019
      supports: SUPPORT
      evidence_source: HUMAN_CLINICAL
      snippet: Scabies and related bacterial skin and soft tissue infections (SSTIs) are highly prevalent in many tropical, low- and middle-income settings.
      explanation: Deep research cited this publication as relevant literature for Scabies.
- reference: DOI:10.1371/journal.pntd.0009661
  title: A framework for scabies control
  found_in:
  - Scabies-deep-research-falcon.md
  findings:
  - statement: Scabies is a neglected tropical disease (NTD) that causes a significant health burden, particularly in disadvantaged communities and where there is overcrowding.
    supporting_text: Scabies is a neglected tropical disease (NTD) that causes a significant health burden, particularly in disadvantaged communities and where there is overcrowding.
    evidence:
    - reference: DOI:10.1371/journal.pntd.0009661
      reference_title: A framework for scabies control
      supports: SUPPORT
      evidence_source: OTHER
      snippet: Scabies is a neglected tropical disease (NTD) that causes a significant health burden, particularly in disadvantaged communities and where there is overcrowding.
      explanation: Deep research cited this publication as relevant literature for Scabies.
- reference: DOI:10.1371/journal.pntd.0012429
  title: 'Quality of life among adults with scabies: A community-based cross-sectional study in north-western Ethiopia'
  found_in:
  - Scabies-deep-research-falcon.md
  findings:
  - statement: Scabies undermines quality of life through its highly disturbing disease symptoms, by distorting self-perception, and secondary to social stigma.
    supporting_text: Scabies undermines quality of life through its highly disturbing disease symptoms, by distorting self-perception, and secondary to social stigma.
    evidence:
    - reference: DOI:10.1371/journal.pntd.0012429
      reference_title: 'Quality of life among adults with scabies: A community-based cross-sectional study in north-western Ethiopia'
      supports: SUPPORT
      evidence_source: HUMAN_CLINICAL
      snippet: Scabies undermines quality of life through its highly disturbing disease symptoms, by distorting self-perception, and secondary to social stigma.
      explanation: Deep research cited this publication as relevant literature for Scabies.
- reference: DOI:10.1371/journal.pntd.0012775
  title: 'The disability-adjusted life years (DALYs), prevalence and incidence of scabies, 1990–2021: A systematic analysis from the Global Burden of Disease Study 2021'
  found_in:
  - Scabies-deep-research-falcon.md
  findings:
  - statement: Current literature lacks a recent global analysis of scabies.
    supporting_text: Current literature lacks a recent global analysis of scabies.
    evidence:
    - reference: DOI:10.1371/journal.pntd.0012775
      reference_title: 'The disability-adjusted life years (DALYs), prevalence and incidence of scabies, 1990–2021: A systematic analysis from the Global Burden of Disease Study 2021'
      supports: SUPPORT
      evidence_source: OTHER
      snippet: Current literature lacks a recent global analysis of scabies.
      explanation: Deep research cited this publication as relevant literature for Scabies.
- reference: DOI:10.1371/journal.pone.0314140
  title: 'Assessment of scabies and its associated factors in Hawassa Zuria District, Southern Ethiopia: A cross-sectional study'
  found_in:
  - Scabies-deep-research-falcon.md
  findings:
  - statement: Scabies is a common but neglected skin disease caused by the parasitic mite Sarcoptes scabiei var. hominis.
    supporting_text: Scabies is a common but neglected skin disease caused by the parasitic mite Sarcoptes scabiei var. hominis.
    evidence:
    - reference: DOI:10.1371/journal.pone.0314140
      reference_title: 'Assessment of scabies and its associated factors in Hawassa Zuria District, Southern Ethiopia: A cross-sectional study'
      supports: SUPPORT
      evidence_source: HUMAN_CLINICAL
      snippet: Scabies is a common but neglected skin disease caused by the parasitic mite Sarcoptes scabiei var. hominis.
      explanation: Deep research cited this publication as relevant literature for Scabies.
- reference: DOI:10.3389/fimmu.2023.1128688
  title: 'Commentary: Transcriptome analysis of host inflammatory responses to the ectoparasitic mite Sarcoptes scabiei var. hominis'
  found_in:
  - Scabies-deep-research-falcon.md
  findings: []
- reference: DOI:10.3389/fitd.2024.1429266
  title: 'Scabies: current knowledge and future directions'
  found_in:
  - Scabies-deep-research-falcon.md
  findings:
  - statement: Scabies is a global public health issue, with approximately 455 million new cases worldwide each year.
    supporting_text: Scabies is a global public health issue, with approximately 455 million new cases worldwide each year.
    evidence:
    - reference: DOI:10.3389/fitd.2024.1429266
      reference_title: 'Scabies: current knowledge and future directions'
      supports: SUPPORT
      evidence_source: OTHER
      snippet: Scabies is a global public health issue, with approximately 455 million new cases worldwide each year.
      explanation: Deep research cited this publication as relevant literature for Scabies.
- reference: DOI:10.3389/frhs.2024.1279762
  title: 'Cost-effectiveness of mass drug administration for control of scabies in Ethiopia: a decision-analytic model'
  found_in:
  - Scabies-deep-research-falcon.md
  findings:
  - statement: The strategies to control scabies in highly endemic populations include individual case/household management and mass drug administration (MDA).
    supporting_text: The strategies to control scabies in highly endemic populations include individual case/household management and mass drug administration (MDA).
    evidence:
    - reference: DOI:10.3389/frhs.2024.1279762
      reference_title: 'Cost-effectiveness of mass drug administration for control of scabies in Ethiopia: a decision-analytic model'
      supports: SUPPORT
      evidence_source: OTHER
      snippet: The strategies to control scabies in highly endemic populations include individual case/household management and mass drug administration (MDA).
      explanation: Deep research cited this publication as relevant literature for Scabies.
- reference: DOI:10.3390/jcm13185511
  title: 'Escalating Threat of Drug-Resistant Human Scabies: Current Insights and Future Directions'
  found_in:
  - Scabies-deep-research-falcon.md
  findings:
  - statement: Scabies is a prevalent dermatological condition with significant public health implications.
    supporting_text: Scabies is a prevalent dermatological condition with significant public health implications.
    evidence:
    - reference: DOI:10.3390/jcm13185511
      reference_title: 'Escalating Threat of Drug-Resistant Human Scabies: Current Insights and Future Directions'
      supports: SUPPORT
      evidence_source: OTHER
      snippet: Scabies is a prevalent dermatological condition with significant public health implications.
      explanation: Deep research cited this publication as relevant literature for Scabies.
- reference: PMID:35298417
  title: "Scabies: update on treatment and efforts for prevention and control in highly endemic settings."
  findings: []
- reference: PMID:30755943
  title: "An Itchy Problem: A Clinical Case of Crusted Scabies."
  findings: []
- reference: PMID:34925353
  title: Transcriptome Analysis of Host Inflammatory Responses to the Ectoparasitic Mite Sarcoptes scabiei var. hominis.
  findings: []
- reference: PMID:23940705
  title: Sarcoptes scabiei mites modulate gene expression in human skin equivalents.
  findings: []
datasets:
- accession: geo:GSE178563
  title: Transcriptome analysis of the host immune responses to Sarcoptes scabiei
  description: Scabies is a human skin disease due to the burrowing ectoparasite Sarcoptes scabiei resulting in intense itching and inflammation and manifesting as skin allergy. Little is known about the specific scabies molecules and genes involved in the host inflammatory and immunologic responses. We interrogated the transcriptome profiles of skin biopsies using next generation sequencing and a combined clustering and pathway mapping approach which will enable us in the identification of key signaling events in the host immune and inflammatory responses to S. scabiei infestation. With the comprehensive analysis of RNA-seq results, it has been found that the immune response of host inhibits S.
  organism:
    preferred_term: human
    term:
      id: NCBITaxon:9606
      label: Homo sapiens
  data_type: BULK_RNA_SEQ
  sample_count: 8
  publication: PMID:34925353
  notes: Identified by GEO DataSets index search for Scabies (scripts/discover_datasets.py); accession and metadata verified against NCBI E-utilities on 2026-08-01. Title, sample count, and organism are GEO's own values.
  evidence:
  - reference: PMID:34925353
    reference_title: Transcriptome Analysis of Host Inflammatory Responses to the Ectoparasitic Mite Sarcoptes scabiei var. hominis.
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    quote_role: PRIMARY_RESULT
    snippet: 'Here we aimed to interrogate the transcriptomic profiles of mite-infested human skin biopsies with clinical manifestations of ordinary scabies subjects ("OS"; n = 05) and subjects naive to scabies ("control"; n = 03) using RNASeq data analysis.'
    explanation: Primary publication generating the bulk RNA-seq dataset of human ordinary scabies and control skin biopsies.
- accession: geo:GSE48459
  title: Sarcoptes scabiei Mites Modulate Gene Expression In Human Skin Equivalents
  description: The purpose of this study was to identify genes in keratinocytes and fibroblasts in human skin equivalents that changed expression in response to the burrowing of live scabies mites.
  organism:
    preferred_term: human
    term:
      id: NCBITaxon:9606
      label: Homo sapiens
  data_type: MICROARRAY
  sample_count: 14
  publication: PMID:23940705
  notes: Identified by GEO DataSets index search for Scabies (scripts/discover_datasets.py); accession and metadata verified against NCBI E-utilities on 2026-08-01. Title, sample count, and organism are GEO's own values.
  evidence:
  - reference: PMID:23940705
    reference_title: Sarcoptes scabiei mites modulate gene expression in human skin equivalents.
    supports: SUPPORT
    evidence_source: IN_VITRO
    quote_role: PRIMARY_RESULT
    snippet: "The purpose of this study was to identify genes in keratinocytes and fibroblasts in human skin equivalents (HSEs) that changed expression in response to the burrowing of live scabies mites."
    explanation: Primary publication reporting the microarray dataset of human skin equivalents challenged with live burrowing S. scabiei mites.
notes: >-
  Scabies exhibits a striking immunological dichotomy between its two major
  clinical forms: immunocompetent patients with ordinary scabies mount a
  protective, CD4+ T-cell-dominated (4:1 CD4+:CD8+ ratio) Th1 cell-mediated
  response that restricts parasite burden, whereas immunocompromised or elderly
  patients with crusted (Norwegian) scabies develop a non-protective,
  CD8+ T-cell-predominant Th2 allergic response (marked by elevated IL-4, IL-5,
  IL-13, and serum IgE) accompanied by IL-20-associated hyperkeratosis and
  uncontrolled mite proliferation. During primary infestation, live burrowing
  mites actively modulate early host keratinocyte and fibroblast immune
  signaling, producing a characteristic 4-to-8-week asymptomatic incubation
  period before hypersensitivity-driven rash and IL-4/IL-31-mediated pruritus
  emerge. In endemic tropical and overcrowded settings, epidermal breaches from
  mite burrows and scratching frequently lead to secondary Streptococcus
  pyogenes and Staphylococcus aureus impetigo and downstream post-streptococcal
  glomerulonephritis, making two-dose oral ivermectin mass drug administration
  a key public-health intervention.
📚

References & Deep Research

References

19
DOI:10.1007/s00436-024-08173-6
Scabies: Immunopathogenesis and pathological changes
No top-level findings curated for this source.
DOI:10.1007/s00436-024-08298-8
Scabies vaccines: where we stand and challenges ahead
No top-level findings curated for this source.
DOI:10.1101/2024.11.25.24317899
Impact of Scabies on Quality of Life and Recent Advances in Management: A Systematic Review
1 finding
Scabies are a highly transmittable disease of the skin.
"Scabies are a highly transmittable disease of the skin."
Show evidence (1 reference)
DOI:10.1101/2024.11.25.24317899 Preprint · not peer-reviewed SUPPORT Other
"Scabies are a highly transmittable disease of the skin."
Deep research cited this publication as relevant literature for Scabies.
DOI:10.1111/bjd.19170
Estimating the global burden of scabies: what else do we need?*
No top-level findings curated for this source.
DOI:10.1111/jdv.19167
Prevalence of scabies worldwide—An updated systematic literature review in 2022
1 finding
Scabies is a World Health Organization‐defined neglected tropical disease, with continuously rising incidence worldwide in recent years.
"Scabies is a World Health Organization‐defined neglected tropical disease, with continuously rising incidence worldwide in recent years."
Show evidence (1 reference)
DOI:10.1111/jdv.19167 SUPPORT Other
"Scabies is a World Health Organization‐defined neglected tropical disease, with continuously rising incidence worldwide in recent years."
Deep research cited this publication as relevant literature for Scabies.
DOI:10.1111/jdv.19288
Detection of a knockdown mutation in the voltage‐sensitive sodium channel associated with permethrin tolerance in <i>Sarcoptes scabiei</i> var. <i>hominis</i> mites
1 finding
Increasing evidence has sparked a debate on the loss of sensitivity of scabies mites to conventional permethrin therapy.
"Increasing evidence has sparked a debate on the loss of sensitivity of scabies mites to conventional permethrin therapy."
Show evidence (1 reference)
DOI:10.1111/jdv.19288 SUPPORT Other
"Increasing evidence has sparked a debate on the loss of sensitivity of scabies mites to conventional permethrin therapy."
Deep research cited this publication as relevant literature for Scabies.
DOI:10.1371/journal.pgph.0003706
Costs of primary healthcare presentations and hospital admissions for scabies and related skin infections in Fiji, 2018–2019
1 finding
Scabies and related bacterial skin and soft tissue infections (SSTIs) are highly prevalent in many tropical, low- and middle-income settings.
"Scabies and related bacterial skin and soft tissue infections (SSTIs) are highly prevalent in many tropical, low- and middle-income settings."
Show evidence (1 reference)
DOI:10.1371/journal.pgph.0003706 SUPPORT Human clinical
"Scabies and related bacterial skin and soft tissue infections (SSTIs) are highly prevalent in many tropical, low- and middle-income settings."
Deep research cited this publication as relevant literature for Scabies.
DOI:10.1371/journal.pntd.0009661
A framework for scabies control
1 finding
Scabies is a neglected tropical disease (NTD) that causes a significant health burden, particularly in disadvantaged communities and where there is overcrowding.
"Scabies is a neglected tropical disease (NTD) that causes a significant health burden, particularly in disadvantaged communities and where there is overcrowding."
Show evidence (1 reference)
DOI:10.1371/journal.pntd.0009661 SUPPORT Other
"Scabies is a neglected tropical disease (NTD) that causes a significant health burden, particularly in disadvantaged communities and where there is overcrowding."
Deep research cited this publication as relevant literature for Scabies.
DOI:10.1371/journal.pntd.0012429
Quality of life among adults with scabies: A community-based cross-sectional study in north-western Ethiopia
1 finding
Scabies undermines quality of life through its highly disturbing disease symptoms, by distorting self-perception, and secondary to social stigma.
"Scabies undermines quality of life through its highly disturbing disease symptoms, by distorting self-perception, and secondary to social stigma."
Show evidence (1 reference)
DOI:10.1371/journal.pntd.0012429 SUPPORT Human clinical
"Scabies undermines quality of life through its highly disturbing disease symptoms, by distorting self-perception, and secondary to social stigma."
Deep research cited this publication as relevant literature for Scabies.
DOI:10.1371/journal.pntd.0012775
The disability-adjusted life years (DALYs), prevalence and incidence of scabies, 1990–2021: A systematic analysis from the Global Burden of Disease Study 2021
1 finding
Current literature lacks a recent global analysis of scabies.
"Current literature lacks a recent global analysis of scabies."
Show evidence (1 reference)
DOI:10.1371/journal.pntd.0012775 SUPPORT Other
"Current literature lacks a recent global analysis of scabies."
Deep research cited this publication as relevant literature for Scabies.
DOI:10.1371/journal.pone.0314140
Assessment of scabies and its associated factors in Hawassa Zuria District, Southern Ethiopia: A cross-sectional study
1 finding
Scabies is a common but neglected skin disease caused by the parasitic mite Sarcoptes scabiei var. hominis.
"Scabies is a common but neglected skin disease caused by the parasitic mite Sarcoptes scabiei var. hominis."
Show evidence (1 reference)
DOI:10.1371/journal.pone.0314140 SUPPORT Human clinical
"Scabies is a common but neglected skin disease caused by the parasitic mite Sarcoptes scabiei var. hominis."
Deep research cited this publication as relevant literature for Scabies.
DOI:10.3389/fimmu.2023.1128688
Commentary: Transcriptome analysis of host inflammatory responses to the ectoparasitic mite Sarcoptes scabiei var. hominis
No top-level findings curated for this source.
DOI:10.3389/fitd.2024.1429266
Scabies: current knowledge and future directions
1 finding
Scabies is a global public health issue, with approximately 455 million new cases worldwide each year.
"Scabies is a global public health issue, with approximately 455 million new cases worldwide each year."
Show evidence (1 reference)
DOI:10.3389/fitd.2024.1429266 SUPPORT Other
"Scabies is a global public health issue, with approximately 455 million new cases worldwide each year."
Deep research cited this publication as relevant literature for Scabies.
DOI:10.3389/frhs.2024.1279762
Cost-effectiveness of mass drug administration for control of scabies in Ethiopia: a decision-analytic model
1 finding
The strategies to control scabies in highly endemic populations include individual case/household management and mass drug administration (MDA).
"The strategies to control scabies in highly endemic populations include individual case/household management and mass drug administration (MDA)."
Show evidence (1 reference)
DOI:10.3389/frhs.2024.1279762 SUPPORT Other
"The strategies to control scabies in highly endemic populations include individual case/household management and mass drug administration (MDA)."
Deep research cited this publication as relevant literature for Scabies.
DOI:10.3390/jcm13185511
Escalating Threat of Drug-Resistant Human Scabies: Current Insights and Future Directions
1 finding
Scabies is a prevalent dermatological condition with significant public health implications.
"Scabies is a prevalent dermatological condition with significant public health implications."
Show evidence (1 reference)
DOI:10.3390/jcm13185511 SUPPORT Other
"Scabies is a prevalent dermatological condition with significant public health implications."
Deep research cited this publication as relevant literature for Scabies.
PMID:35298417
Scabies: update on treatment and efforts for prevention and control in highly endemic settings.
No top-level findings curated for this source.
PMID:30755943
An Itchy Problem: A Clinical Case of Crusted Scabies.
No top-level findings curated for this source.
PMID:34925353
Transcriptome Analysis of Host Inflammatory Responses to the Ectoparasitic Mite Sarcoptes scabiei var. hominis.
No top-level findings curated for this source.
PMID:23940705
Sarcoptes scabiei mites modulate gene expression in human skin equivalents.
No top-level findings curated for this source.

Deep Research

1

Deep research results are used as seeds for research; they do not undergo the same validation as the main records and may contain errors. How we use deep research.

Falcon ▸
Disease Characteristics Research Template
Edison Scientific Literature 47 citations 2026-04-04T16:23:52.600176

Question: You are an expert researcher providing comprehensive, well-cited information.

Provide detailed information focusing on: 1. Key concepts and definitions with current understanding 2. Recent developments and latest research (prioritize 2023-2024 sources) 3. Current applications and real-world implementations 4. Expert opinions and analysis from authoritative sources 5. Relevant statistics and data from recent studies

Format as a comprehensive research report with proper citations. Include URLs and publication dates where available. Always prioritize recent, authoritative sources and provide specific citations for all major claims.

Disease Characteristics Research Template

Target Disease

  • Disease Name: Scabies
  • MONDO ID: (if available)
  • Category: Infectious Disease

Research Objectives

Please provide a comprehensive research report on Scabies covering all of the disease characteristics listed below. This report will be used to populate a disease knowledge base entry. Be thorough and cite primary literature (PMID preferred) for all claims.

For each section, suggested databases/resources are listed. These are the first places you should search for information on each topic.

1. Disease Information

Search first: OMIM, Orphanet, ICD-10/ICD-11, MeSH, PubMed

  • What is the disease? Provide a concise overview.
  • What are the key identifiers? (OMIM, Orphanet, ICD-10/ICD-11, MeSH, Mondo)
  • What are the common synonyms and alternative names?
  • Is the information derived from individual patients (e.g., EHR) or aggregated disease-level resources?

2. Etiology

  • Disease Causal Factors: What are the primary causes? (genetic, environmental, infectious, mechanistic)
  • Risk Factors:

    Search first: PubMed, Cochrane Library, UpToDate, clinical guidelines, ClinVar, ClinGen, GWAS Catalog, PheGenI, CTD, CDC, WHO, epidemiological databases

  • Genetic risk factors (causal variants, susceptibility loci, modifier genes)
  • Environmental risk factors (toxins, lifestyle, occupational exposures, age, sex, family history)
  • Protective Factors:

    Search first: PubMed, Cochrane Library, clinical trial databases, GWAS Catalog, gnomAD, WHO, CDC, nutrition databases

  • Genetic protective factors (protective variants, modifier alleles)
  • Environmental protective factors (diet, lifestyle, exposures that reduce risk)
  • Gene-Environment Interactions: How do genetic and environmental factors interact to influence disease?

    Search first: CTD, PubMed, PheGenI, GxE databases

3. Phenotypes

Search first: HPO (Human Phenotype Ontology), OMIM, Orphanet, PubMed, clinicaltrials.gov, MedDRA, SNOMED CT, DECIPHER, LOINC

For each phenotype, provide: - Phenotype type: symptoms, clinical signs, physical manifestations, behavioral changes, or laboratory abnormalities

For symptoms/signs: HPO, OMIM, Orphanet, PubMed For behavioral changes: HPO, DSM, RDoC (Research Domain Criteria), PubMed For laboratory abnormalities: LOINC, SNOMED CT, LabTests Online, PubMed - Phenotype characteristics: Search first: OMIM, Orphanet, HPO, PubMed - Age of symptom onset (neonatal, childhood, adult-onset, late-onset) - Symptom severity (mild, moderate, severe, variable) - Symptom progression (stable, progressive, episodic, fluctuating) - Frequency among affected individuals (percentage or qualitative) - Quality of life impact: Effects on daily functioning and well-being (per-phenotype when possible) Search first: EQ-5D database, SF-36, WHO QOL databases, PubMed - Suggest HPO (Human Phenotype Ontology) terms for each phenotype

4. Genetic/Molecular Information

  • Causal Genes: Gene mutations or chromosomal abnormalities responsible for disease (gene symbols, OMIM IDs)

    Search first: OMIM, ClinVar, HGMD, Ensembl, NCBI Gene

  • Pathogenic Variants:
  • Affected genes (gene symbols, HGNC IDs) > Search first: OMIM, NCBI Gene, Ensembl, HGNC, UniProt, GeneCards
  • Variant classification (pathogenic, likely pathogenic, VUS per ACMG/AMP guidelines) > Search first: ClinVar, ClinGen, ACMG/AMP guidelines, VarSome
  • Variant type/class (missense, frameshift, nonsense, splice-site, structural)
  • Allele frequency in population databases > Search first: gnomAD, 1000 Genomes, ExAC, TOPMed, dbSNP
  • Somatic vs germline origin > Search first: COSMIC (somatic), ClinVar, ICGC, TCGA
  • Functional consequences (loss of function, gain of function, dominant negative)
  • Modifier Genes: Genes that modify disease severity or expression
  • Epigenetic Information: DNA methylation, histone modifications, chromatin changes affecting disease

    Search first: ENCODE, Roadmap Epigenomics, MethBase, DiseaseMeth

  • Chromosomal Abnormalities: Large-scale genetic changes (aneuploidy, translocations, inversions)

    Search first: DECIPHER, ClinVar, ECARUCA, UCSC Genome Browser

5. Environmental Information

  • Environmental Factors: Non-genetic contributing factors (toxins, radiation, pollution, occupational exposure)

    Search first: CTD (Comparative Toxicogenomics Database), TOXNET, PubMed, EPA databases

  • Lifestyle Factors: Behavioral factors (smoking, diet, exercise, alcohol consumption)

    Search first: CDC databases, WHO, PubMed, NHANES

  • Infectious Agents: If applicable, pathogens causing or triggering disease (bacteria, viruses, fungi, parasites)

    Search first: NCBI Taxonomy, ViPR, BV-BRC, MicrobeDB, GIDEON

6. Mechanism / Pathophysiology

  • Molecular Pathways: Specific signaling cascades or biochemical pathways involved (Wnt, MAPK, mTOR, PI3K-AKT, etc.)

    Search first: KEGG, Reactome, WikiPathways, PathBank, BioCyc

  • Cellular Processes: Cell-level mechanisms (apoptosis, autophagy, cell cycle dysregulation, inflammation, etc.)

    Search first: Gene Ontology (GO), Reactome, KEGG, PubMed

  • Protein Dysfunction: How protein structure or function is altered (misfolding, aggregation, loss of function, gain of function)

    Search first: UniProt, PDB (Protein Data Bank), InterPro, Pfam, AlphaFold

  • Metabolic Changes: Alterations in metabolic processes (energy metabolism, lipid metabolism, amino acid metabolism)

    Search first: KEGG, BioCyc, HMDB (Human Metabolome Database), BRENDA

  • Immune System Involvement: Role of immune response (autoimmunity, immunodeficiency, chronic inflammation)

    Search first: ImmPort, Immunome Database, IEDB, Gene Ontology

  • Tissue Damage Mechanisms: How tissues/ are injured (oxidative stress, ischemia, fibrosis, necrosis)

    Search first: PubMed, Gene Ontology, Reactome

  • Biochemical Abnormalities: Specific molecular defects (enzyme deficiencies, receptor dysfunction, ion channel defects)

    Search first: BRENDA, UniProt, KEGG, OMIM, PubMed

  • Epigenetic Changes: DNA methylation, histone modifications affecting gene expression in disease

    Search first: ENCODE, Roadmap Epigenomics, MethBase, DiseaseMeth

  • Molecular Profiling (if available):
  • Transcriptomics/gene expression changes > Search first: GEO (Gene Expression Omnibus), ArrayExpress, GTEx, Human Cell Atlas, SRA
  • Proteomics findings > Search first: PRIDE, ProteomeXchange, Human Protein Atlas, STRING, BioGRID
  • Metabolomics signatures > Search first: MetaboLights, Metabolomics Workbench, HMDB, METLIN
  • Lipidomics alterations > Search first: LIPID MAPS, SwissLipids, LipidHome, Metabolomics Workbench
  • Genomic structural features > Search first: UCSC Genome Browser, Ensembl, NCBI, dbVar, DGV
  • Advanced Technologies (if applicable):
  • Single-cell analysis findings (cell-type specific mechanisms, cellular heterogeneity) > Search first: Human Cell Atlas, Single Cell Portal, GEO, CELLxGENE
  • Spatial transcriptomics findings > Search first: GEO, Spatial Research, Vizgen, 10x Genomics data
  • Multi-omics integration results > Search first: TCGA, ICGC, cBioPortal, LinkedOmics, PubMed
  • Functional genomics screens (CRISPR, RNAi) > Search first: DepMap, GenomeRNAi, PubMed, BioGRID ORCS

For each mechanism, describe: - The causal chain from initial trigger to clinical manifestation - Which mechanisms are upstream vs downstream - What cell types and biological processes are involved - Suggest GO terms for biological processes and CL terms for cell types

7. Anatomical Structures Affected

  • Organ Level:
  • Primary organs directly affected
  • Secondary organ involvement (complications, secondary effects)
  • Body systems involved (cardiovascular, nervous, digestive, respiratory, endocrine, etc.)

    Search first: Uberon, FMA (Foundational Model of Anatomy), OMIM, HPO, ICD-11, MeSH, SNOMED CT

  • Tissue and Cell Level:
  • Specific tissue types affected (epithelial, connective, muscle, nervous)
  • Specific cell populations targeted (with Cell Ontology terms)

    Search first: Uberon, Human Protein Atlas, Cell Ontology, Human Cell Atlas, CellMarker, PanglaoDB

  • Subcellular Level:
  • Cellular compartments involved (mitochondria, nucleus, ER, lysosomes) (with GO Cellular Component terms)

    Search first: Gene Ontology (Cellular Component), UniProt, Human Protein Atlas

  • Localization:
  • Specific anatomical sites (with UBERON terms) > Search first: FMA, Uberon, NeuroNames (for brain), SNOMED CT
  • Lateralization (unilateral, bilateral, asymmetric) > Search first: HPO, clinical literature, imaging databases

8. Temporal Development

  • Onset:
  • Typical age of onset (congenital, pediatric, adult, geriatric)
  • Onset pattern (acute, subacute, chronic, insidious)

    Search first: OMIM, Orphanet, HPO, PubMed

  • Progression:
  • Disease stages (early, intermediate, advanced, end-stage) > Search first: Cancer Staging Manual (AJCC), WHO classifications, PubMed
  • Progression rate (rapid, slow, variable)
  • Disease course pattern (episodic, relapsing-remitting, progressive, stable)
  • Disease duration (self-limited, chronic lifelong)

    Search first: Disease registries, longitudinal cohort databases, natural history studies, PubMed, Orphanet, OMIM

  • Patterns:
  • Remission patterns (spontaneous, treatment-induced) > Search first: Clinical trial databases, disease registries, PubMed
  • Critical periods (time windows of vulnerability or opportunity for intervention) > Search first: PubMed, developmental biology databases, clinical guidelines

9. Inheritance and Population

  • Epidemiology:
  • Prevalence (cases per 100,000 at given time)
  • Incidence (new cases per 100,000 per year)

    Search first: Orphanet, CDC, WHO, GBD (Global Burden of Disease), national registries, SEER, disease registries

  • For Genetic Etiology:
  • Inheritance pattern (AD, AR, X-linked, mitochondrial, multifactorial, polygenic) > Search first: OMIM, Orphanet, ClinVar, GTR (Genetic Testing Registry)
  • Penetrance (complete, incomplete, age-dependent) > Search first: ClinVar, OMIM, PubMed, ClinGen
  • Expressivity (variable, consistent) > Search first: OMIM, ClinVar, PubMed
  • Genetic anticipation (increasing severity in successive generations) > Search first: OMIM, PubMed (especially for repeat expansion disorders)
  • Germline mosaicism > Search first: ClinVar, OMIM, genetic counseling literature, PubMed
  • Founder effects (population-specific mutations) > Search first: gnomAD, population genetics databases, PubMed
  • Consanguinity role > Search first: OMIM, population studies, genetic counseling resources
  • Carrier frequency > Search first: gnomAD, carrier screening databases, GeneReviews, GTR
  • Population Demographics:
  • Affected populations (ethnic or demographic groups with higher prevalence) > Search first: gnomAD, 1000 Genomes, PAGE Study, PubMed, population registries
  • Geographic distribution (endemic areas, regional variation) > Search first: WHO, CDC, GBD, Orphanet, geographic epidemiology databases
  • Geographic distribution of specific variants
  • Sex ratio (male:female) > Search first: Disease registries, OMIM, PubMed, epidemiological databases
  • Age distribution of affected individuals > Search first: CDC, disease registries, SEER, Orphanet

10. Diagnostics

  • Clinical Tests:
  • Laboratory tests (blood, urine, tissue chemistry, specific enzyme assays) > Search first: LOINC, LabTests Online, PubMed
  • Biomarkers (proteins, metabolites, genetic markers, circulating biomarkers) > Search first: FDA Biomarker List, BEST (Biomarkers, EndpointS, and other Tools), PubMed
  • Imaging studies (X-ray, CT, MRI, PET, ultrasound) > Search first: RadLex, DICOM, Radiopaedia, imaging databases
  • Functional tests (pulmonary function, cardiac stress tests) > Search first: LOINC, clinical guidelines, PubMed
  • Electrophysiology (EEG, EMG, ECG, nerve conduction studies) > Search first: LOINC, clinical neurophysiology databases, PubMed
  • Biopsy findings (histopathology, immunohistochemistry) > Search first: SNOMED CT, College of American Pathologists resources, PubMed
  • Pathology findings (microscopic examination) > Search first: SNOMED CT, Digital Pathology databases, PubMed
  • Genetic Testing:

    Search first: GTR (Genetic Testing Registry), GeneReviews, ClinGen

  • Overview of recommended genetic testing approach
  • Whole genome sequencing (WGS) utility > Search first: GTR, ClinVar, GEL (Genomics England), gnomAD
  • Whole exome sequencing (WES) utility > Search first: GTR, ClinVar, OMIM, GeneMatcher
  • Gene panels (which panels, which genes) > Search first: GTR, ClinVar, laboratory-specific databases
  • Single gene testing > Search first: GTR, ClinVar, OMIM, GeneReviews
  • Chromosomal microarray (CMA) > Search first: DECIPHER, ClinVar, dbVar, ECARUCA
  • Karyotyping > Search first: Chromosome Abnormality Database, ClinVar, cytogenetics resources
  • FISH > Search first: ClinVar, cytogenetics databases, PubMed
  • Mitochondrial DNA testing > Search first: MITOMAP, MSeqDR, ClinVar, GTR
  • Repeat expansion testing > Search first: GTR, ClinVar, repeat expansion databases, PubMed
  • Omics-Based Diagnostics (if applicable):
  • RNA sequencing / transcriptomics > Search first: GEO, ArrayExpress, GTEx, RNA-seq databases
  • Proteomics > Search first: PRIDE, ProteomeXchange, FDA Biomarker database
  • Metabolomics > Search first: MetaboLights, Metabolomics Workbench, HMDB
  • Epigenomics > Search first: GEO, ENCODE, Roadmap Epigenomics, MethBase
  • Liquid biopsy > Search first: COSMIC, ClinVar, liquid biopsy databases, PubMed
  • Clinical Criteria:
  • Standardized diagnostic criteria (DSM, ICD, society guidelines) > Search first: DSM-5, ICD-11, clinical society guidelines, UpToDate
  • Differential diagnosis (other conditions to rule out, with distinguishing features) > Search first: DynaMed, UpToDate, clinical decision support systems
  • Screening:
  • Screening methods for asymptomatic individuals (newborn screening, carrier screening, cascade screening) > Search first: ACMG recommendations, CDC newborn screening, GTR

11. Outcome/Prognosis

  • Survival and Mortality:
  • Survival rate (5-year, 10-year, overall) > Search first: SEER, cancer registries, disease-specific registries, PubMed
  • Life expectancy (with and without treatment if applicable) > Search first: Orphanet, disease registries, actuarial databases, PubMed
  • Mortality rate > Search first: CDC, WHO, GBD, national mortality databases
  • Disease-specific mortality (deaths directly attributable to disease) > Search first: Disease registries, CDC Wonder, GBD, PubMed
  • Morbidity and Function:
  • Morbidity (disease-related disability and health impacts) > Search first: GBD, WHO, disability databases, PubMed
  • Disability outcomes (long-term functional impairments) > Search first: ICF (International Classification of Functioning), disability registries
  • Quality of life measures (EQ-5D, SF-36, PROMIS, disease-specific tools) > Search first: EQ-5D database, SF-36, PROMIS, PubMed
  • Disease Course:
  • Complications (secondary problems: infections, organ failure, etc.) > Search first: ICD codes, disease registries, clinical databases, PubMed
  • Recovery potential (likelihood and extent of recovery, with vs without treatment) > Search first: Natural history studies, rehabilitation databases, PubMed
  • Prediction:
  • Prognostic factors (age, disease severity, biomarkers, treatment response) > Search first: Prognostic models databases, clinical calculators, PubMed
  • Prognostic biomarkers (molecular markers predicting disease course) > Search first: FDA Biomarker database, PubMed, cancer prognostic databases

12. Treatment

  • Pharmacotherapy:
  • Pharmacological treatments (drug names, drug classes, mechanisms of action) > Search first: DrugBank, RxNorm, ATC classification, DailyMed, FDA databases
  • Pharmacogenomics (how genetic variants affect drug metabolism, efficacy, toxicity) > Search first: PharmGKB, CPIC (Clinical Pharmacogenetics), FDA Table of PGx Biomarkers
  • Advanced Therapeutics:
  • Gene therapy (viral vectors, CRISPR, gene replacement, gene editing) > Search first: ClinicalTrials.gov, FDA gene therapy database, ASGCT resources
  • Cell therapy (stem cell transplant, CAR-T, cellular therapeutics) > Search first: ClinicalTrials.gov, FDA cell therapy database, FACT standards
  • RNA-based therapies (ASOs, siRNA, mRNA therapies) > Search first: ClinicalTrials.gov, FDA approvals, PubMed
  • Targeted therapies (treatments directed at specific molecular targets) > Search first: My Cancer Genome, OncoKB, ClinicalTrials.gov, FDA approvals
  • Immunotherapies (checkpoint inhibitors, monoclonal antibodies) > Search first: Cancer Immunotherapy Database, FDA approvals, ClinicalTrials.gov
  • Surgical and Interventional:
  • Surgical interventions (types of surgery, timing, outcomes) > Search first: CPT codes, surgical registries, clinical guidelines, PubMed
  • Supportive and Rehabilitative:
  • Supportive care (symptom management, pain control, nutrition) > Search first: Clinical guidelines, Cochrane Library, PubMed
  • Rehabilitation (physical therapy, occupational therapy, speech therapy) > Search first: Rehabilitation medicine databases, clinical guidelines, PubMed
  • Experimental:
  • Experimental treatments in clinical trials (with NCT identifiers if available) > Search first: ClinicalTrials.gov, EU Clinical Trials Register, WHO ICTRP
  • Treatment Outcomes:
  • Treatment response rates > Search first: Clinical trial databases, FDA reviews, systematic reviews, PubMed
  • Side effects and adverse events > Search first: FDA Adverse Event Reporting System (FAERS), MedWatch, PubMed
  • Treatment Strategy:
  • Treatment algorithms (clinical pathways, decision trees) > Search first: Clinical practice guidelines, NCCN Guidelines, UpToDate
  • Combination therapies > Search first: ClinicalTrials.gov, treatment guidelines, PubMed
  • Personalized medicine approaches (genotype-guided treatment) > Search first: My Cancer Genome, CIViC, PharmGKB, precision medicine databases

For each treatment, suggest MAXO (Medical Action Ontology) terms where applicable.

13. Prevention

  • Prevention Levels:
  • Primary prevention (preventing disease occurrence: vaccination, risk factor modification) > Search first: CDC, WHO, USPSTF recommendations, Cochrane Library
  • Secondary prevention (early detection and treatment: screening programs, early intervention) > Search first: USPSTF, CDC screening guidelines, WHO
  • Tertiary prevention (preventing complications in those with disease) > Search first: Clinical guidelines, disease management protocols, PubMed
  • Immunization: Vaccine strategies (if applicable)

    Search first: CDC vaccine schedules, WHO immunization, FDA vaccine database

  • Screening and Early Detection:
  • Screening programs (population-based: newborn screening, cancer screening) > Search first: CDC screening programs, USPSTF, cancer screening databases
  • Genetic screening (carrier screening, preimplantation genetic diagnosis, prenatal testing) > Search first: ACMG recommendations, ACOG guidelines, GTR
  • Risk stratification (identifying high-risk individuals for targeted prevention) > Search first: Risk prediction models, clinical calculators, PubMed
  • Behavioral Interventions: Lifestyle modifications to reduce risk

    Search first: CDC, WHO, behavioral intervention databases, Cochrane Library

  • Counseling: Genetic counseling (risk assessment, family planning guidance)

    Search first: NSGC resources, ACMG guidelines, GeneReviews

  • Public Health:
  • Public health interventions (sanitation, vector control, health education) > Search first: CDC, WHO, public health databases, PubMed
  • Environmental interventions (reducing environmental risk factors) > Search first: EPA databases, WHO environmental health, PubMed
  • Prophylaxis: Preventive medications or procedures

    Search first: Clinical guidelines, FDA approvals, PubMed

14. Other Species / Natural Disease

  • Taxonomy: Species affected (with NCBI Taxon identifiers)

    Search first: NCBI Taxonomy

  • Breed: Specific breeds affected (with VBO identifiers if applicable)

    Search first: VBO (Vertebrate Breed Ontology)

  • Gene: Orthologous genes in other species (with NCBI Gene IDs)

    Search first: NCBI Gene

  • Natural Disease:
  • Naturally occurring disease in other species (companion animals, wildlife) > Search first: OMIA (Online Mendelian Inheritance in Animals), VetCompass, PubMed
  • Veterinary relevance and importance in animal health > Search first: OMIA, veterinary databases, PubMed
  • Comparative Biology:
  • Comparative pathology (similarities and differences across species) > Search first: OMIA, comparative pathology databases, PubMed
  • Evolutionary conservation of disease mechanisms > Search first: HomoloGene, OrthoMCL, Alliance of Genome Resources
  • Transmission (if applicable):
  • Zoonotic potential > Search first: CDC zoonotic diseases, WHO zoonoses, GIDEON
  • Cross-species susceptibility > Search first: NCBI Taxonomy, veterinary databases, PubMed

15. Model Organisms

  • Model Types:
  • Model organism type (mammalian, invertebrate, cellular, in vitro) > Search first: Alliance of Genome Resources, model organism databases
  • Specific model systems (mouse, rat, zebrafish, Drosophila, C. elegans, yeast, cell lines, organoids, iPSCs) > Search first: MGI, RGD, ZFIN, FlyBase, WormBase, SGD, ATCC, Cellosaurus
  • Induced models (drug treatment, surgical intervention, environmental manipulation) > Search first: MGI, model organism databases, PubMed
  • Genetic Models:
  • Types available (knockout, knock-in, transgenic, conditional, humanized) > Search first: MGI, IMPC, KOMP, EuMMCR, IMSR
  • Model Characteristics:
  • Phenotype recapitulation (how well model reproduces human disease features) > Search first: Model organism databases, comparative studies, PubMed
  • Model limitations (aspects of human disease not captured) > Search first: Model organism databases, PubMed, review articles
  • Applications:
  • Research applications (what aspects of disease can be studied) > Search first: Model organism databases, PubMed
  • Resources:
  • Model databases > Search first: MGI, RGD, ZFIN, FlyBase, WormBase, IMSR, EMMA, MMRRC

Citation Requirements

  • Cite primary literature (PMID preferred) for all mechanistic and clinical claims
  • Prioritize recent reviews and landmark papers
  • Include direct quotes from abstracts where possible to support key statements
  • Distinguish evidence source types: human clinical, model organism, in vitro, computational

Output Format

Structure your response as a comprehensive narrative organized by the sections above. For each section, provide: - Factual content with specific details (numbers, percentages, gene names, variant nomenclature) - Ontology term suggestions (HPO, GO, CL, UBERON, CHEBI, MAXO, MONDO) where applicable - Evidence citations with PMIDs - Direct quotes from abstracts to support key claims - Clear indication when information is not available or not applicable for this disease

This report will be used to populate a disease knowledge base entry with: - Pathophysiology descriptions with causal chains - Gene/protein annotations (HGNC, GO terms) - Phenotype associations (HP terms) with frequencies - Cell type involvement (CL terms) - Anatomical locations (UBERON terms) - Chemical entities (CHEBI terms) - Treatment annotations (MAXO terms) - Evidence items with PMIDs and exact abstract quotes - Epidemiology, prognosis, diagnostic, and prevention information - Animal model descriptions with phenotype recapitulation details

Scabies — Comprehensive Disease Characteristics Report (2023–2024 prioritized)

Target disease

  • Disease name: Scabies
  • Category: Infectious disease (ectoparasitic infestation)
  • Causal agent: Sarcoptes scabiei var. hominis (mite) (mitchell2024scabiescurrentknowledge pages 1-2, schneider2023prevalenceofscabies pages 1-2)
  • MONDO ID: Not retrieved from the tool-accessible literature set in this run (gap).

1. Disease information

Concise overview (current understanding)

Scabies is a parasitic skin disease caused by infestation with the mite Sarcoptes scabiei var. hominis, characterized clinically by pruritus and typical lesion distributions, and it can lead to secondary bacterial skin infections such as impetigo. (mitchell2024scabiescurrentknowledge pages 1-2, li2024thedisabilityadjustedlife pages 1-2)

WHO/NTD status: Scabies was added to the WHO neglected tropical diseases (NTD) portfolio in 2017, and it is included in NTD control discussions and targets toward 2030. (mitchell2024scabiescurrentknowledge pages 1-2, sharaf2024scabiesvaccineswhere pages 1-2)

Key identifiers (ontology / coding)

  • IACS (International Alliance for the Control of Scabies) diagnostic framework: Three diagnostic certainty levels are widely referenced: confirmed, clinical, suspected. (engelman2021aframeworkfor pages 2-4, li2024thedisabilityadjustedlife pages 1-2)
  • ICD / MeSH / MONDO: Not reliably extractable from the retrieved evidence set in this run; should be populated from ICD/MeSH/MONDO registries directly (gap).

Common synonyms / alternative names

  • Crusted scabies is also described as Norwegian scabies in clinical and guideline literature. (simonart2024escalatingthreatof pages 1-5)

Evidence source type

Most content here is derived from aggregated disease-level resources (systematic reviews, WHO/NTD frameworks, GBD analyses, guidelines) rather than individual EHR-only sources. (li2024thedisabilityadjustedlife pages 1-2, engelman2021aframeworkfor pages 2-4, mitchell2024scabiescurrentknowledge pages 1-2)

2. Etiology

Primary cause

Infestation by Sarcoptes scabiei var. hominis; gravid females burrow in the stratum corneum and lay eggs; clinical manifestations are driven largely by host inflammatory/hypersensitivity responses. (mitchell2024scabiescurrentknowledge pages 1-2, engelman2021aframeworkfor pages 2-4, sharaf2024scabiesimmunopathogenesisand pages 4-6)

Transmission (infectious / environmental)

Direct skin-to-skin contact is the primary route; indirect transmission via contaminated items is possible but less prominent. (li2024thedisabilityadjustedlife pages 1-2, mitchell2024scabiescurrentknowledge pages 1-2)

Timing: Symptom onset can be delayed in first infestation (up to 4–8 weeks), and more rapid (days) with prior exposure. (mitchell2024scabiescurrentknowledge pages 1-2)

Risk factors (recent and authoritative)

Consistent risk factors across recent reviews and epidemiologic studies include: - Overcrowding / communal living (e.g., schools, prisons, aged care facilities, refugee camps) (mitchell2024scabiescurrentknowledge pages 1-2, li2024thedisabilityadjustedlife pages 1-2) - Poverty / low socioeconomic status and limited access to clean water (li2024thedisabilityadjustedlife pages 1-2, dejen2024assessmentofscabies pages 1-2) - Immunosuppression (increases risk of crusted scabies and major transmission) (mitchell2024scabiescurrentknowledge pages 1-2, simonart2024escalatingthreatof pages 1-5)

Quantified risk factor evidence (example; community study): In southern Ethiopia (Sept–Nov 2023 survey), scabies odds were higher with low/middle wealth index, overcrowding index >1.5, unimproved water source, washing hands with water only, and sleeping on the floor. (dejen2024assessmentofscabies pages 1-2)

Protective factors (emerging)

A case-control study in southwest Ethiopia reported higher daily household water consumption (≥25 L per person/day) as strongly protective (AOR 0.06). (dejen2024assessmentofscabies pages 2-4)

Genetic risk/protective factors & gene–environment interaction

Scabies is not primarily a Mendelian genetic disease; however, host immune genetic variation may influence susceptibility. A 2024 study of 154 patients (Iraq; 2022–2023) reported cytokine polymorphism associations including IL-10 GA genotype protective (OR 0.61) and IL-13 TT genotype associated with susceptibility (OR 2.14). (sharaf2024scabiesimmunopathogenesisand pages 2-4)

Interpretation: these findings suggest a gene–environment interaction where exposure (crowding/contact) intersects with host immune regulation (Th2/anti-inflammatory cytokine pathways) to shape risk and/or severity, but replication across populations is needed. (sharaf2024scabiesimmunopathogenesisand pages 2-4, sharaf2024scabiesimmunopathogenesisand pages 4-6)

3. Phenotypes

Core phenotypes (symptoms/signs) and suggested HPO terms

Below are common scabies phenotypes with ontology suggestions; frequencies vary by setting.

1) Pruritus (often worse at night) - Type: Symptom - Characteristics: often severe; may cause insomnia and impaired QoL; particularly prominent in ordinary scabies (li2024thedisabilityadjustedlife pages 1-2, dejen2024assessmentofscabies pages 1-2) - HPO: Pruritus (HP:0000989); Insomnia (HP:0100785)

2) Papules / vesicles / pustules in characteristic sites (interdigital spaces, wrists, elbows, etc.) - Type: Clinical signs - Characteristic distribution: interdigital spaces, flexor wrists, elbows reported as frequent sites in a 2023 community survey (dejen2024assessmentofscabies pages 1-2) - HPO: Papule (HP:0200033), Vesicle (HP:0200042), Pustule (HP:0000967)

3) Burrows - Type: Physical manifestation - Role: key diagnostic clue used in simplified mapping/exam approaches (mitchell2024scabiescurrentknowledge pages 5-6) - HPO: Skin burrow (not always represented as a single HPO term; map to scabies-specific phenotype extensions if needed)

4) Crusted (Norwegian) scabies - Type: Severe clinical subtype - Characteristics: hyperkeratotic/crusted lesions, very high mite burden; may be less itchy; major outbreak risk; associated with immunosuppression or debility (simonart2024escalatingthreatof pages 1-5) - HPO: Hyperkeratosis (HP:0000962), Palmoplantar keratoderma (HP:0000982) (clinical examples supported by crusted scabies descriptions and histopathology) (sharaf2024scabiesimmunopathogenesisand media 34ad7ec0)

Severity and quality-of-life (QoL) impact

A community-based study in north-western Ethiopia (2024; 86 adults with scabies) found mean DLQI 9.2 (SD 7.6) (moderate impairment). 54.7% had moderate/severe QoL impact and 27% reported extremely severe impact; the most affected domains were “symptoms and feelings” and “daily activity”. (yirgu2024qualityoflife pages 1-2, yirgu2024qualityoflife pages 5-7)

4. Genetic / molecular information

Causal genes

Not applicable in the Mendelian sense: scabies is caused by a parasite rather than an inherited human gene defect. (mitchell2024scabiescurrentknowledge pages 1-2)

Parasite molecular mechanisms relevant to drug response (key recent development)

Permethrin tolerance/resistance via target-site mutation: Riebenbauer et al. (JEADV; July 2023; https://doi.org/10.1111/jdv.19288) reported a VGSC/VSSC “kdr-type” mutation M918L in S. scabiei var. hominis, detected in 97.0% (65/67) mites sampled from 64 patients in their dataset; the paper states the mutation “is associated with resistance of the kdr type”. (riebenbauer2023detectionofa pages 3-4, riebenbauer2023detectionofa pages 6-7)

Implication: This supports a plausible genetic basis for declining permethrin effectiveness in at least some settings and motivates resistance surveillance. (riebenbauer2023detectionofa pages 1-2)

5. Environmental information

Environmental/lifestyle contributors

Crowded living conditions and limited access to water/hygiene resources repeatedly emerge as key determinants (global review + local surveys). (mitchell2024scabiescurrentknowledge pages 1-2, dejen2024assessmentofscabies pages 1-2)

Infectious agents and co-infections

Scabies is itself an infestation; a major downstream effect is predisposition to bacterial SSTIs. Scabies-associated skin barrier disruption and immune modulation can increase risk of impetigo and other pyoderma; mites and burrows may harbor bacteria including Staphylococcus aureus and group A streptococci. (sharaf2024scabiesimmunopathogenesisand pages 7-8)

6. Mechanism / pathophysiology

High-level causal chain (current understanding)

1) Mite infestation and burrowing in the stratum corneum → deposition of mite products/antigens. (mitchell2024scabiescurrentknowledge pages 1-2, sharaf2024scabiesimmunopathogenesisand pages 4-6) 2) Innate immune activation in epidermis (keratinocytes, dendritic cells/Langerhans cells) and antigen presentation to lymph nodes → adaptive responses. (sharaf2024scabiesimmunopathogenesisand pages 2-4) 3) Inflammatory infiltrates (eosinophils, mast cells, basophils, macrophages, neutrophils) and cytokine production → pruritus and dermatitis. (sharaf2024scabiesimmunopathogenesisand pages 2-4, sharaf2024scabiesimmunopathogenesisand pages 7-8) 4) Excoriation + barrier injury + mite-mediated complement/immune modulation → secondary bacterial infection risk and systemic sequelae in some contexts. (sharaf2024scabiesimmunopathogenesisand pages 6-7, sharaf2024scabiesimmunopathogenesisand pages 7-8)

Ordinary vs crusted scabies: immune polarization

Sharaf (Parasitology Research; March 2024; https://doi.org/10.1007/s00436-024-08173-6) synthesizes evidence that: - Ordinary scabies is associated with Th1-type responses (IFN-γ, TNF-α, IL-2). (sharaf2024scabiesimmunopathogenesisand pages 4-6) - Crusted scabies is associated with Th2-skewed cytokines (IL-4, IL-5, IL-13; also IL-31) and dysregulated cellular immunity; Th17 axis involvement is also implicated, particularly when IL-10 is reduced and Treg/Th17 balance is disrupted. (sharaf2024scabiesimmunopathogenesisand pages 4-6, sharaf2024scabiesimmunopathogenesisand pages 6-7)

Mite immune evasion mechanisms described include complement inhibition (serine protease inhibitors blocking complement pathways) and induction of anti-inflammatory mediators such as IL-10 and IL-1 receptor antagonist. (sharaf2024scabiesimmunopathogenesisand pages 6-7, sharaf2024scabiesvaccineswhere pages 1-2)

Suggested ontology terms

  • GO biological process (examples): inflammatory response; T cell activation; type I hypersensitivity; complement activation; keratinocyte proliferation (supported by described cytokines/immune infiltrates and crusted scabies hyperkeratosis) (sharaf2024scabiesimmunopathogenesisand pages 4-6, sharaf2024scabiesimmunopathogenesisand pages 7-8)
  • Cell Ontology (CL) (examples): keratinocyte; Langerhans cell; dendritic cell; CD4-positive, αβ T cell; CD8-positive T cell; eosinophil; mast cell; neutrophil (sharaf2024scabiesimmunopathogenesisand pages 2-4, sharaf2024scabiesimmunopathogenesisand pages 4-6)

Visual evidence (figure/table)

  • A schematic summarizing immunopathogenesis and mite/host interactions (Sharaf 2024, Figure 3) is available (sharaf2024scabiesimmunopathogenesisand media 29abd1ed).
  • Histopathology showing crusted scabies with heavy mite infestation and hyperkeratosis (Sharaf 2024, Figure 2) is available (sharaf2024scabiesimmunopathogenesisand media 34ad7ec0).

7. Anatomical structures affected

Primary structures

  • Skin (epidermis/stratum corneum) is the primary site of mite burrowing and immune response. (mitchell2024scabiescurrentknowledge pages 1-2, sharaf2024scabiesimmunopathogenesisand pages 4-6)

Tissue/cell level

  • Epidermal keratinocytes and antigen-presenting cells (dendritic/Langerhans) initiate and shape immune responses; dermis shows mixed inflammatory infiltrates. (sharaf2024scabiesimmunopathogenesisand pages 2-4, sharaf2024scabiesimmunopathogenesisand pages 7-8)

UBERON suggestions

  • Skin (UBERON:0002097)
  • Epidermis (UBERON:0001003)
  • Stratum corneum (UBERON:0002068)

8. Temporal development

  • Onset pattern: delayed after first infestation (weeks) but rapid with reinfestation (days). (mitchell2024scabiescurrentknowledge pages 1-2)
  • Course: can be persistent without treatment; crusted scabies may progress with massive mite burden and prolonged undiagnosed periods, increasing outbreak risk. (simonart2024escalatingthreatof pages 1-5)

9. Inheritance and population

Global epidemiology (recent statistics)

A systematic analysis of scabies burden using GBD 2021 data (PLOS NTD; Dec 2024; https://doi.org/10.1371/journal.pntd.0012775) estimated that in 2021 scabies caused: - 5.3 million DALYs - 206.6 million prevalent cases - 622.5 million incident cases with burden concentrated in tropical regions and particularly affecting children and young people. (li2024thedisabilityadjustedlife pages 1-2)

Prevalence range in population-based surveys

A 2023 systematic review (JEADV; May 2023; https://doi.org/10.1111/jdv.19167) included 43 population-based studies and reported very wide prevalence variation, including 71.0% in five Ghanaian communities and 76.9% in an Indonesian boarding school (children-only study), with a low of 0.18% in Uganda. (schneider2023prevalenceofscabies pages 1-2)

High-risk settings

Congregate settings (schools, prisons, aged-care facilities, refugee camps) and overcrowded housing are repeatedly cited as high-risk contexts. (mitchell2024scabiescurrentknowledge pages 1-2)

10. Diagnostics

Clinical criteria / standardized case definitions

  • The 2020 IACS criteria provide standardized diagnostic certainty strata (confirmed/clinical/suspected) and are recommended as a standard for surveys and programs. (engelman2021aframeworkfor pages 2-4, cox2021estimatingtheglobal pages 5-9)
  • A community study in Ethiopia explicitly applied IACS diagnostic criteria for prevalence estimation and risk-factor analysis. (dejen2024assessmentofscabies pages 1-2)

Confirmatory tests

  • Microscopy of skin scrapings remains a reference standard for confirmation by identifying mites/eggs/feces, but may be impractical and have limited sensitivity in field use. (cox2021estimatingtheglobal pages 5-9, engelman2021aframeworkfor pages 2-4)

Newer/advanced diagnostic approaches (recent synthesis)

A 2024 systematic review (preprint) summarizes increased use of noninvasive imaging (dermoscopy, video dermoscopy, reflectance confocal microscopy, optical coherence tomography) and PCR assays for mite DNA as diagnostic advances. (kumari2024titleimpactof pages 28-32, kumari2024titleimpactof pages 1-4)

Differential diagnosis (high-level)

Differential diagnosis often includes other pruritic dermatoses (e.g., eczema/dermatitis) and other infestations; standardized criteria and confirmatory testing help reduce misclassification. (cox2021estimatingtheglobal pages 5-9)

LOINC/SNOMED-style test mapping (suggestions)

Not directly retrievable from the provided evidence set; suggested mapping targets include “skin scraping microscopy for mite/egg/scybala” and “PCR for Sarcoptes scabiei DNA,” to be aligned with local laboratory coding systems. (cox2021estimatingtheglobal pages 5-9, kumari2024titleimpactof pages 28-32)

11. Outcome / prognosis

Complications and morbidity

  • Scabies can predispose to impetigo and other SSTIs, with downstream severe outcomes in some settings (including cellulitis, lymphangitis, acute glomerulonephritis; rarely death), especially in crusted scabies with fissures and heavy infestation. (sharaf2024scabiesimmunopathogenesisand pages 7-8, simonart2024escalatingthreatof pages 1-5)

Quality of life (recent data)

As above (DLQI study; 2024 Ethiopia): mean DLQI 9.2; 27% extremely severe QoL impact. (yirgu2024qualityoflife pages 1-2, yirgu2024qualityoflife pages 5-7)

Health-system economic burden (real-world implementation)

Fiji national extrapolation from Big SHIFT surveillance (PLOS Global Public Health; Oct 2024; https://doi.org/10.1371/journal.pgph.0003706) estimated: - US$3.0 million annual direct healthcare costs attributable to scabies and related SSTIs (~US$3.3 per capita) - US$17.7 average cost per primary healthcare presentation for scabies - US$439 average cost per hospital admission for potentially scabies-related SSTI (akpan2024costsofprimary pages 1-2)

12. Treatment

Standard pharmacotherapy and regimens (current practice)

A 2024 review summarizing current practice describes: - Topical permethrin 5%: whole-body application for 8–12 hours; often repeated after 7–14 days. (mitchell2024scabiescurrentknowledge pages 5-6) - Oral ivermectin: active against mites but not eggs; short half-life necessitating repeat dosing 7–14 days apart; generally avoided in pregnancy and children <15 kg in many guidelines. (mitchell2024scabiescurrentknowledge pages 5-6) - Benzyl benzoate: topical alternative used in some programs/guidelines. (mitchell2024scabiescurrentknowledge pages 5-6)

Comparative effectiveness: A 2018 Cochrane review is summarized as finding no difference between permethrin and ivermectin in efficacy. (mitchell2024scabiescurrentknowledge pages 5-6)

Mass drug administration (MDA) as a public-health control strategy

Evidence syntheses emphasize MDA as effective in highly endemic settings. - A 2024 scabies control review describes strong evidence including a Fiji trial with 94% reduction (32% to <2%) at 12 months and a meta-analysis with relative reductions 79% for scabies and 66% for impetigo. (mitchell2024scabiescurrentknowledge pages 6-7) - A scabies control framework recommends piloting MDA at community prevalence ≥10%, with suggested stopping threshold <2% and a commonly used regimen two doses ivermectin 200 μg/kg 7–14 days apart (and topical alternatives for ineligible groups). (engelman2021aframeworkfor pages 4-5)

Drug resistance (major 2023–2024 development)

  • Molecular evidence: kdr-type VGSC mutation M918L associated with permethrin tolerance in human scabies mites (2023). (riebenbauer2023detectionofa pages 6-7, riebenbauer2023detectionofa pages 3-4)
  • Programmatic implication: the need for resistance monitoring and potential alternative strategies, including combination regimens and investigation of new oral agents. (mitchell2024scabiescurrentknowledge pages 6-7)

Emerging therapeutics / future directions

Moxidectin is highlighted as a promising oral alternative with longer half-life and potential for single-dose treatment, relevant to improving MDA feasibility and adherence. (mitchell2024scabiescurrentknowledge pages 6-7)

Treatment ontology suggestions (MAXO)

  • Topical antiparasitic therapy (permethrin application)
  • Systemic antiparasitic therapy (oral ivermectin)
  • Mass drug administration (community-wide ivermectin-based MDA)
  • Contact tracing and treatment of close contacts (these are conceptual MAXO mappings; exact IDs should be selected from MAXO catalog during curation). (mitchell2024scabiescurrentknowledge pages 5-6, engelman2021aframeworkfor pages 4-5)

Clinical trials (real-world pipeline; selected)

  • NCT04332068 (University of Oxford; Phase 2; started 2023-11-18; completed 2025-04-04): oral ivermectin vs permethrin in children 5 to <15 kg (includes dose escalation up to 800 μg/kg at some sites); primary outcome adverse events; includes population PK and WGS pharmacogenomics. (NCT04332068 chunk 1, NCT04332068 chunk 2)
  • NCT05819983 (Universitas Padjadjaran; Phase 4; completed 2023): compares 3-dose ivermectin vs 2-dose ivermectin vs permethrin 5% (days 1 and 8) in ≥6 years/≥15 kg; outcomes include lesion severity and pruritus (5 weeks); no results posted in the record excerpt. (NCT05819983 chunk 1)
  • NCT07145736 (Kirby Institute; recruiting; Angola; includes scabies among conditions): moxidectin vs ivermectin for MDA in onchocerciasis/other NTDs; operational eligibility information provided; no results posted. (NCT07145736 chunk 2)

13. Prevention

Individual and household prevention

Key prevention principles include rapid case identification and simultaneous treatment of close/household contacts, plus environmental measures (laundering/drying linens/clothes) that may help but have limited evidence. (mitchell2024scabiescurrentknowledge pages 5-6, mitchell2024scabiescurrentknowledge pages 6-7)

Community-level prevention (MDA thresholds)

WHO-aligned frameworks recommend: - individual/household management for prevalence <10% - community-wide MDA where prevalence is ≥10% (mitchell2024scabiescurrentknowledge pages 6-7, engelman2021aframeworkfor pages 4-5)

Cost-effectiveness threshold evidence (2024)

A decision-analytic model for Ethiopia (Frontiers in Health Services; Sep 2024; https://doi.org/10.3389/frhs.2024.1279762) found ivermectin-based MDA to be cost-effective in a base case (population 100,000; prevalence 15%) and suggested initiating MDA at prevalence >10%; MDA was not cost-effective below 10% prevalence or when effectiveness <85%. (hounsome2024costeffectivenessofmass pages 1-2)

14. Other species / natural disease

Scabies-like infestation occurs in many mammals ("sarcoptic mange"), but cross-species taxonomy, zoonotic potential, and OMIA/NCBI taxon details were not retrievable from the current evidence set and should be populated from veterinary/parasitology resources (gap).

15. Model organisms

Porcine models are used for mechanistic studies and transcriptomics; a 2023 commentary summarizes that transcriptomic analyses support Th2 signatures in both ordinary and crusted scabies and increased IL-17 pathway magnitude in crusted disease, with time-dependent immune activation patterns. (mounsey2023commentarytranscriptomeanalysis pages 2-3)

Expert opinions / analysis (authoritative synthesis)

Recent authoritative syntheses converge on several expert-level conclusions: 1) Standardized diagnosis is essential for burden estimation and control planning; IACS criteria address longstanding inconsistencies and enable mapping strategies. (cox2021estimatingtheglobal pages 5-9, engelman2021aframeworkfor pages 2-4) 2) MDA is among the most impactful control tools for high-prevalence settings, but two-dose ivermectin schedules and contraindicated groups constrain implementation; longer-acting oral agents could be transformative. (mitchell2024scabiescurrentknowledge pages 6-7, engelman2021aframeworkfor pages 4-5) 3) Resistance surveillance is now a priority: molecular evidence (VGSC kdr mutation) supports a plausible biologic basis for permethrin tolerance, reinforcing the need for monitoring and diversified treatment approaches. (riebenbauer2023detectionofa pages 6-7, mitchell2024scabiescurrentknowledge pages 6-7)

Abstract-quotable statements (verbatim snippets available from retrieved texts)

  • GBD 2021 (PLOS NTD; Dec 2024): “In 2021, scabies caused 5.3 million DALYs, 206.6 million prevalence, and 622.5 million incidence …” (as quoted in the evidence extraction). (li2024thedisabilityadjustedlife pages 1-2)
  • Riebenbauer 2023 (JEADV; Jul 2023): M918L mutation “is associated with resistance of the kdr type.” (riebenbauer2023detectionofa pages 6-7)

Limitations / gaps in this run

  • Ontology IDs (MONDO, MeSH, ICD-10/ICD-11) were not directly retrievable from the tool-accessible literature set and should be supplemented from dedicated ontology registries.
  • Some “latest” sources (e.g., certain 2024 BJD meta-analyses and Nature Reviews Disease Primers) were flagged as unobtainable in the search results and therefore could not be cited here.

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