A thickened patch on a giraffe’s leg is easy to recognise as a skin problem. Explaining how it began is harder. The same damaged surface may contain parasites, inflammatory cells and signs of healing, but their presence alone does not reveal the order in which they arrived. To understand a disease, researchers need to connect what they can see on the animal with what is happening inside its skin.
J. Wanda, E. Mjingo, E. Mwega and J. Malago investigated that connection in Masai giraffes in Tanzania’s Ruaha National Park. Their 2025 paper in Veterinary Medicine International combined microscope examinations with DNA analysis. It moved the investigation from a broad suspicion that parasitic worms were involved towards genetic evidence about the worms found in particular lesions.
The work provides a more specific lead in an unresolved problem. It also shows why identifying a parasite is one stage of explaining a disease, rather than the end of the investigation.
Beneath a damaged surface
Giraffe skin disease is a descriptive name for a condition involving abnormal patches of skin. In the Tanzanian animals discussed by the researchers, lesions can involve hair loss, crusting and thickened tissue, often on the forelimbs. A visible lesion describes what has happened to the skin; it does not by itself identify the organism or process responsible.
Wanda and colleagues obtained small skin biopsies from ten affected giraffes, five of each sex, during GPS-tagging work in October and November 2022. The animals were selected for examination with the severity and position of their lesions in mind. The team worked with sampling support from the Tanzania Wildlife Research Institute’s REGROW project, and the specimens were analysed at Sokoine University of Agriculture.
This design made it possible to examine diseased tissue closely. It was not a random sample of all Ruaha giraffes, and it did not include an equivalent set of unaffected animals. Any fraction of positive samples therefore describes these ten selected cases, rather than the proportion of the park’s giraffes carrying the parasite.
The researchers used two complementary views. Thin tissue sections allowed them to look for organisms and the skin’s response around them. DNA analysis could then help place an organism among its relatives, even when the microscope alone could not settle its identity.
Six biopsies contained worm larvae
Microscopy revealed larvae of spirurid nematodes in six of the ten biopsies. Nematodes are roundworms; spirurids are a broad grouping within them. The larvae lay within the dermis, the skin layer beneath the surface, including tissue around hair follicles.
Their position matters. These were organisms located within the damaged tissue, alongside inflammatory cells and other abnormalities. The sections also showed clear spaces around some larvae and increased fibrous tissue. Fibrosis is the laying down of connective tissue during repair, which can leave skin thickened and altered.
The microscope therefore brought the suspect and the injury into the same view. It gave the researchers a reason to investigate a parasitic contribution rather than relying only on the outward appearance of the lesions.
It could not establish that the worms initiated every lesion. A tissue section is a very thin slice through a much larger patch. Failing to see a worm in one biopsy may reflect its distribution or the stage of the lesion. Conversely, seeing a worm in damaged skin does not exclude an earlier injury or another process contributing to the condition.
A DNA comparison sharpens the identification
The team took the six samples positive on microscopy forward for DNA analysis. Three produced a positive result for the genetic region they targeted. This is an important sequence of numbers: ten giraffes were sampled, six biopsies contained visible larvae, and three of those six yielded the DNA signal used for the molecular investigation.
The researchers examined part of 28S ribosomal DNA, a stretch of genetic material that can be compared across related organisms. A close sequence match can help narrow an unknown worm’s relatives, much as comparing a passage of inherited instructions can reveal which known versions it most resembles.
The sequence most closely matched reference sequences labelled Thelazia callipaeda, with similarities of approximately 99.1% and 99.4%. In the paper’s evolutionary comparison, the giraffe-associated sequence grouped with those references. That was a more specific result than observing a roundworm-shaped structure under a microscope.
The authors described the organism as Thelazia and, in their conclusion, as T. callipaeda. The direct result is the close match across the partial DNA region examined. It is not a comparison of complete genomes, and it does not establish that the giraffe parasite shares every aspect of the reference species’ biology.
That distinction is particularly useful here. Thelazia is associated with eyeworms, while these samples came from skin lesions. A genetic relationship creates a question about identity and tissue location; it does not show how an organism usually associated with one part of the body reached another. The researchers did not identify a transmission route into giraffe skin.
Why the family tree still needs more branches
A related investigation shows why additional genetic regions and reference species can matter. In a 2023 study of skin lesions in 22 cattle in Texas, Clinson C. Lui, Matthew Kulpa, Guilherme G. Verocai and colleagues characterised the skin parasite Stephanofilaria stilesi. They combined microscopy with several genetic markers.
Their comparisons suggested that Stephanofilaria was more closely related to the broader eyeworm group, Thelazioidea, than its traditional classification implied. A worm associated with skin lesions could therefore sit near eyeworm relatives in a genetic comparison. That finding does not identify the Ruaha parasite as Stephanofilaria. It explains why a fuller comparison, with more genes and more candidate relatives, could be informative before treating one close match as a complete biological identification.
The cattle study also found that microscopy and DNA tests did not always identify the same positive specimens. Tissue selection, preservation and the distribution of parasites can affect what each method detects. The two approaches answer connected questions and can compensate for one another’s blind spots.
For the giraffe investigation, their combination is the main advance: organisms could be placed in injured skin, and a genetic sequence could be linked to the investigation of those lesions. Further work can now examine both their identity and their association with the disease more precisely.
From a parasite’s presence to its role
Wanda and colleagues recommended studying a broader range of samples from affected and unaffected animals, with more extensive genetic characterisation. That comparison would address a central missing question: are these worms consistently associated with diseased skin, or can they also occur without the condition?
Finding a stronger association with lesions would support a role in disease, while the pattern in unaffected skin would help interpret the meaning of a positive test. Sampling remains a constraint. A small biopsy represents one place at one time, and collecting comparable material from wild giraffes is an undertaking that depends on appropriate veterinary and conservation work.
Another useful comparison would follow lesions through their development. If parasites are found in early changes before extensive thickening appears, that would tell a different story from their appearance mainly in older, already damaged tissue. Repeated observations could also show whether the number of visible worms changes as a lesion heals. These are ways to investigate the order of events without assuming it from the final appearance.
Transmission is a further question. The study did not establish which animal or insect, if any, carries the parasite between hosts. A plausible relative in a DNA database cannot identify a local carrier. Evidence connecting parasites from giraffes with potential carriers would be needed to turn that possibility into an explanation.
The Ruaha findings give giraffe health research a clearer organism to investigate and a clearer distinction to preserve. Worms were present in some sampled lesions, and their DNA narrowed the search for their relatives. Understanding whether they start the skin disease, worsen an existing lesion or participate in a more complicated process is the next part of the story.
Sources
J. Wanda, E. Mjingo, E. Mwega and J. Malago. “Identification and Molecular Characterization of Spirurid Nematode Associated With Giraffe Skin Disease in Ruaha National Park, Tanzania.” Veterinary Medicine International, article 5053029 (2025). DOI: 10.1155/vmi/5053029. Read the open-access paper · Research-library record.
Clinson C. Lui, Matthew Kulpa, Guilherme G. Verocai, Aníbal G. Armién, Erin E. Edwards, Dominique J. Wiener and Raquel R. Rech. “Reassessing Stephanofilaria stilesi dermatitis in cattle, with characterization of molecular markers for confirming diagnosis.” Parasites & Vectors 16, 278 (2023). DOI: 10.1186/s13071-023-05905-y. Read the open-access paper.
