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History: An estimated 700 Western gulls (Larus occidentalis) were found dead over a 7-month period in three coastal California counties. Four juvenile gulls found weak and not standing were euthanized and submitted to the U.S. Geological Survey National Wildlife Health Center (NWHC) for cause of death determination. 

Gross Findings:

One of the four examined gulls is a 960 g juvenile male Western gull in fair body condition. Multifocally on the intestinal serosa are numerous ~1-mm diameter firm white nodules; nodules are frequently associated with 1-2.5 cm long orange metazoan parasites extending from the lumen through the intestinal wall (Fig. 1). Large numbers of similar parasites are throughout the intestinal lumen and firmly adhered to the mucosal surface. Additionally, throughout all air sacs and overlying the ventral aspects of the lungs are multifocal to coalescing pinpoint to 5 x 7 cm white to dark green plaques. These plaques are suggestive of fungal pneumonia and airsacculitis; Aspergillus sp. was subsequently detected on fungal culture. For more information regarding aspergillosis, explore the NWHC February 2021 Pathology Case of the Month: Aspergillosis in Mallard Ducks.

Intestinal serosa from a Western gull showing Acanthocephaliasis.
Figure 1. Photographs from a Western gull (Larus occidentalis) in California, USA. (A) On the intestinal serosa are multifocal 1-mm diameter firm white nodules (arrows). A white fungal plaque (white arrow) also overlies the serosa. (B) Numerous orange metazoan parasites (arrow) are throughout the duodenal lumen and multifocally extending to the serosa (arrowheads).

Histopathological Findings: 

Expanding the small intestinal lumen of one of four gulls are multiple metazoan parasites. Parasites have a smooth cuticle and a thick hypodermal layer lined with lacunar channels. Occasionally, parasites exhibit a spined proboscis and corresponding lemnisci. Adjacent small intestinal villi are markedly distorted and multifocally eroded. Parasites are multifocally within cavitations expanding the intestinal serosa; these parasites are multifocally degenerate and surrounded by low numbers of multinucleated giant cells, epithelioid macrophages, and hypereosinophilic (necrotic) debris.

Photomicrographs of the small intestine from a Western gull showing parasites in intestinal wall.
Figure 2. Photomicrographs of the small intestine from a Western gull (Larus occidentalis) from California, USA. H & E stain. (A) Expanding the small intestinal lumen and distorting intestinal villi are multiple adult metazoan parasites (arrow); similar parasites are within cavitations in the intestinal wall or serosa (arrowhead). (B) Worms are unsegmented with a smooth tegument (arrow), a thick hypodermal layer with lacunar channels (arrowhead), and lemnisci with lemnisci compressor muscles at the periphery (asterisks). (C) The anterior portion of the parasite contains a proboscis lined with spines (arrows). (D) Parasites within the intestinal wall or serosa are occasionally surrounded multifocally by low numbers of multinucleated giant cells, epithelioid macrophages, and hypereosinophilic debris (arrows).

Morphologic Diagnoses:

  1. Enteritis, granulomatous, multifocal, moderate, chronic, with intramural and serosal acanthocephalans.

Disease: Acanthocephaliasis

Etiology: Acanthocephalan (thorny-headed worm)

Distribution: Worldwide

Seasonality: Although birds may be infected year-round, many transmission cycles begin in the spring (spring recruitment cycle) with the preponderance of transmission between invertebrates and vertebrates occurring in summer and early fall. Intensity of infections may increase in situations where birds are feeding on heavily infected food items such as in pools with dwindling water and crowding of vertebrate and invertebrate hosts. Seasonality of food items and bird migration are also drivers of transmission. 

Host range: All vertebrate classes are susceptible to acanthocephalan infection; however, waterfowl, including ducks, geese, and swans, are commonly reported final hosts.

Transmission: Acanthocephalans have an indirect life cycle requiring at least one intermediate host. Birds become infected by ingesting crustacea and terrestrial insects (intermediate hosts) or fish, snakes, and frogs (paratenic hosts) which contain the developing juvenile cystacanth stage. Once consumed by the definitive host, the cystacanth then develops into an adult male or female acanthocephalan which mate and release eggs into the birds’ intestines. Eggs are shed into the environment through the feces, where they are ingested by the intermediate host.

Clinical signs: There are often no clinical signs, but lethargy, emaciation, and death may be observed in severe cases.

Pathology: Parasitized birds demonstrate damage to the intestinal tract as acanthocephalans attach to the intestinal wall via a retractable proboscis and absorb nutrients through their integument. Based on worm abundance, varying degrees of blunting and destruction of the villi within the small intestines is observed with erosion of the mucosal epithelium. Cellular infiltration and hemorrhage within the surrounding epithelium and stromal connective tissue is also seen. In severe cases, the worms may obstruct the intestinal tract or penetrate through the intestinal wall with resulting peritonitis.

Diagnosis: Presumptive diagnosis can be made at necropsy by detection of acanthocephala embedded in and protruding through the intestinal wall. Definitive diagnosis may be obtained by gross examination of worms, molecular diagnostics such as polymerase chain reaction (PCR), or microscopically by identifying the characteristic tegument or lemnisci, a muscular structure associated with a retractable proboscis that is specific to the phylum Acanthocephala.

Public health concerns: While zoonotic infection due to exposure to infected birds is unlikely, there are species of acanthocephalans that infect humans through consumption of undercooked or raw fish.

Wildlife population impacts: Acanthocephalans are rarely the cause of primary disease, with pathogenesis heavily influenced by host nutritional status and other environmental stressors. Although it is infrequent, small-scale outbreaks in wildlife populations have been reported, including mortality events in hatch year gull species. At low levels, parasite burdens in general can exacerbate impacts of other stressors, such as seasonal weather extremes, food scarcities, and other disease processes. Thus, it is common for diseased wildlife to be afflicted by multiple opportunistic pathogens as seen in this gull with aspergillosis.

Management: Control in wildlife can be difficult and impractical as there are numerous intermediate hosts prevalent in various ecosystems. To reduce consumption of the cystacanth, efforts can be made to reduce aggregation of birds and crustaceans.


  • Atkinson, CT, Thomas, NJ, Hunter, DB (Eds.). 2009. Parasitic diseases of wild birds. John Wiley & Sons. 
  • Gardiner CH, Poynton SL. 1999. An atlas of metazoan parasites in animal tissues. Armed Forces Institute of Pathology.
  • La Sala LF, Martorelli SR. Intestinal Acanthocephaladiosis in Olrog's gulls (Larus atlanticus): Profilicollis chasmagnathi as possible cause of death. 2007. J Wildl Dis. 2007 Apr;43(2):269-73.
  • Mathison, BA, Mehta, N, Couturier, MR. 2021. Human acanthocephaliasis: A thorn in the side of parasite diagnostics. Journal of Clinical Microbiology, 59(11), 10-1128.
  • Nemeth MN, Yabsley MJ. 2021. SCWDS Field Manual of Wildlife Diseases in the Southeastern United States, 4th Edition. Southeastern Cooperative Wildlife Disease Study. 
  • U.S. Geological Survey National Wildlife Health Center. 2021. Aspergillosis in Mallard Ducks. Accessed April 2024. 
  • U.S. Geological Survey. 1999. Field manual of wildlife diseases: general field procedures and diseases of birds, Accessed April 2024. 

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