Whirling Disease

Whirling disease is a devastating parasitic condition caused by the myxozoan parasite Myxobolus cerebralis, which primarily affects salmonid fish species including trout and salmon. This microscopic parasite targets the cartilage and nervous system of young fish, causing severe neurological damage that results in the characteristic whirling or tail-chasing swimming behavior from which the disease derives its name. First identified in Europe in the late nineteenth century, whirling disease has since spread to numerous countries worldwide, causing significant ecological and economic damage to both wild and farmed salmonid populations. The disease represents one of the most serious parasitic threats to trout and salmon fisheries globally.

The parasite has a complex two-host life cycle requiring both a salmonid fish host and a tubifex worm intermediate host to complete its development. This complicated life cycle means the disease can establish persistent populations in affected waterways, making eradication extremely difficult once the parasite becomes established in an ecosystem. Young fish under five months of age are most susceptible to severe disease, as their cartilage has not yet ossified into bone, providing the soft tissue environment the parasite requires for reproduction. Older fish with fully developed skeletal systems are more resistant to infection but can still carry and spread the parasite.

The impact of whirling disease on fish health extends far beyond the obvious swimming abnormalities. Infected fish develop skeletal deformities including shortened opercula, misshapen heads, and severely curved spines that compromise their ability to feed, evade predators, and maintain normal physiological functions. The neurological damage caused by the parasite destroying cartilage around the auditory and equilibrium organs leads to the characteristic spinning behavior that makes affected fish highly vulnerable to predation and unable to maintain position in currents. Mortality rates among young infected fish can approach one hundred percent in severe outbreaks, devastating both hatchery operations and wild populations.

Early detection and prevention are critical because there is no effective treatment for whirling disease once fish become infected. The parasite spores are extremely resilient, capable of surviving in sediment for decades and resisting most disinfection methods. Management strategies focus on preventing introduction of the parasite to unaffected waters, controlling tubifex worm populations where possible, and maintaining hatchery biosecurity protocols. Understanding the disease and implementing proper prevention measures remains the only effective approach to protecting vulnerable salmonid populations from this destructive parasite.

The primary cause of whirling disease is infection with Myxobolus cerebralis, a microscopic myxozoan parasite that belongs to a group of organisms originally classified as protozoans but now recognized as highly derived cnidarians. The parasite produces two types of spores during its life cycle, each designed to infect a different host species. Myxospores released from infected fish sink to the substrate where they can remain viable for up to thirty years, waiting to be consumed by tubifex worms. Inside the tubifex worm, the parasite transforms and produces triactinomyxon spores, which are released into the water and can actively penetrate the skin of susceptible fish within seconds of contact.

Water quality and environmental factors play crucial roles in the prevalence and severity of whirling disease outbreaks. The tubifex worm intermediate host thrives in sediment-rich environments with high organic matter content, meaning waters with excessive silt, decomposing vegetation, or nutrient pollution often harbor larger tubifex populations and consequently higher parasite loads. Water temperature significantly affects both the parasite's development rate and the fish's susceptibility, with infections progressing most rapidly at temperatures between twelve and seventeen degrees Celsius. Colder waters slow parasite development but also extend the duration of the vulnerable period for young fish.

Environmental and tank factors in aquaculture settings can dramatically influence disease transmission and severity. Facilities using surface water sources from affected watersheds face continuous exposure risk, while recirculating systems can concentrate parasites if tubifex worms become established in biofilters or settling tanks. Earthen ponds with natural substrates provide ideal habitat for tubifex worms, creating ongoing infection pressure. Overcrowding increases stress and pathogen exposure, while poor water flow allows spores to accumulate in areas where fish congregate.

Risk factors for whirling disease include any introduction of fish, equipment, or water from affected sources to uncontaminated facilities or waterways. The parasite can spread through stocking of infected fish, transfer of contaminated water or mud on boots and equipment, movement of infected tubifex worms in aquatic plants or substrate, and even through bird predators that may carry viable spores in their digestive systems. Fish that survive infection become carriers, releasing millions of spores as their infected cartilage degrades, perpetuating the disease cycle in affected waters.

The disease mechanism involves triactinomyxon spores penetrating fish skin and migrating through the peripheral nervous system toward the cartilage of the head and spine. The parasite preferentially targets areas of active cartilage growth, where it multiplies rapidly and destroys tissue essential for proper skeletal development. The destruction of cartilage surrounding the organs of balance and hearing in the inner ear causes the neurological dysfunction responsible for the whirling behavior. As infected cartilage breaks down, millions of myxospores are released, eventually reaching the water when fish die or are consumed by predators, completing the cycle when spores settle to the substrate and contact tubifex worms.

Early warning signs of whirling disease can be subtle and easily overlooked, particularly in young fry where abnormal behavior might be attributed to normal developmental variation. Initial behavioral changes include increased startle responses, difficulty maintaining position in water currents, and slight irregularities in swimming patterns. Affected fish may show reduced feeding activity before obvious symptoms develop, and careful observation might reveal fish swimming at unusual angles or having difficulty orienting themselves properly. Early detection requires vigilant monitoring of young salmonids, particularly during the first few months of life when cartilage infection is most active.

The most recognizable symptom of whirling disease is the characteristic tail-chasing or spinning behavior that gives the disease its common name. Infected fish swim in tight circles or spiral patterns, unable to maintain directional control due to damage to their balance and equilibrium organs. This whirling behavior becomes more pronounced when fish are startled or stressed, often triggering rapid spinning episodes that can last from seconds to minutes. The spinning is involuntary and exhausting, leaving affected fish weakened and unable to compete for food or escape predators. Not all infected fish display whirling behavior, as symptoms depend on the severity and location of cartilage damage.

Behavioral changes associated with whirling disease extend beyond the spinning itself to include a range of abnormalities reflecting neurological impairment. Infected fish often exhibit flashing behavior, repeatedly rubbing against tank surfaces or substrate in apparent response to neurological irritation. Loss of appetite is common as fish become unable to effectively locate and capture food. Affected individuals frequently isolate themselves from schooling groups and may be found resting on the bottom or hiding in corners, conserving energy due to their compromised condition. Swimming may appear labored or uncoordinated even when active whirling is not occurring.

Physical signs of whirling disease develop as the parasite destroys cartilage and the fish's skeleton develops abnormally. Skeletal deformities include severely curved spines producing a hunched or twisted appearance, shortened or deformed gill covers that may expose gill tissue, and compressed or misshapen heads particularly around the jaw and cranium. Darkening of the tail region, called black tail, occurs due to nerve damage affecting pigment cell regulation and is a hallmark sign in young salmonids. The combination of skeletal deformities and darkened tail provides strong presumptive evidence of whirling disease even before laboratory confirmation.

Symptom progression in whirling disease correlates with the extent of cartilage damage and typically worsens over time in severely affected fish. Fish infected at a very young age when cartilage is most abundant tend to develop the most severe deformities, while those infected later when more cartilage has ossified into bone may show milder signs. As skeletal deformities become more pronounced, fish lose the ability to feed effectively due to jaw malformation and swimming impairment. Weight loss and emaciation follow as metabolic demands cannot be met. The combination of starvation, exhaustion from constant spinning, and vulnerability to predation leads to progressive decline.

Emergency symptoms requiring immediate intervention include fish exhibiting constant uncontrolled spinning, complete inability to feed, severe respiratory distress related to opercular deformities, and signs of secondary infections taking advantage of the compromised condition. Groups of young fish showing simultaneous onset of spinning behavior or high mortality with characteristic deformities indicate a serious outbreak requiring immediate biosecurity measures to prevent spread. Fish found dead on the bottom with curved spines and black tails should trigger immediate investigation and testing, as early confirmation allows implementation of containment protocols before the disease spreads further.

Visual examination provides initial diagnostic clues for whirling disease based on the characteristic clinical signs and behavioral abnormalities. Observation of the spinning behavior, skeletal deformities, and black tail syndrome in young salmonids strongly suggests whirling disease, though these signs are not absolutely definitive. Physical examination should assess spinal curvature, head and jaw symmetry, gill cover development, and overall body condition. Examining multiple fish from an affected population helps establish the pattern of disease and distinguishes whirling disease from individual developmental abnormalities. However, visual diagnosis alone cannot confirm whirling disease, as other conditions can cause similar signs.

Water testing, while not directly diagnostic for whirling disease, provides essential context for understanding the environmental conditions that may be facilitating disease transmission. Assessing water source, checking for tubifex worm presence in substrate samples, and documenting water temperature history helps evaluate infection risk. Unlike many fish diseases where water quality problems are the primary cause, whirling disease occurs independently of water chemistry parameters. However, conditions favoring tubifex worm proliferation such as high organic matter and silty substrates indicate elevated risk. Testing incoming water sources for triactinomyxon spores using filtration and microscopy can identify contaminated supplies.

Microscopy and laboratory tests are essential for definitive whirling disease diagnosis. Examination of cartilage samples from the head or spine under the microscope can reveal the characteristic myxospores of Myxobolus cerebralis, which have a distinctive polar capsule arrangement visible with appropriate staining. The pepsin-trypsin digest method processes fish tissue to concentrate and identify spores and remains a standard diagnostic technique. Polymerase chain reaction testing provides highly sensitive and specific detection of parasite DNA, allowing identification of infections before spores are visible and enabling testing of water and sediment samples for environmental contamination. Histopathology reveals characteristic cartilage lesions and parasite stages in tissue sections.

Differential diagnosis must consider other conditions causing similar neurological signs or skeletal abnormalities in salmonids. Viral hemorrhagic septicemia and infectious hematopoietic necrosis can cause spiral swimming, though these typically present with hemorrhage and higher acute mortality. Nutritional deficiencies, particularly tryptophan or ascorbic acid deficiency, can cause skeletal deformities but not the characteristic whirling behavior. Other myxozoan parasites may cause nervous system signs but produce different spore morphology. Physical trauma, genetic abnormalities, and exposure to certain toxins can produce spinal deformities without the progressive neurological deterioration seen in whirling disease. Laboratory confirmation using PCR or spore identification is essential for accurate diagnosis and appropriate management response.

Water quality optimization, while not treating the parasitic infection itself, provides the foundation for supporting affected fish and preventing secondary complications. Maintaining excellent water quality reduces stress on infected fish and supports their immune function during the disease course. Temperature management within the cooler end of the species' tolerance range may slow parasite development, though this also slows fish growth and extends the vulnerable period. Ensuring adequate oxygenation is particularly important as fish with opercular deformities may have compromised gill function. While water quality measures cannot eliminate the parasite, they help maximize survival rates among less severely affected individuals.

There are currently no effective medications that can treat established Myxobolus cerebralis infections in fish. The parasite's intracellular location within cartilage tissue protects it from most antiparasitic drugs, and the damage to cartilage is irreversible once it occurs. Various treatments have been attempted experimentally including fumagillin, which shows activity against some myxozoan parasites, but results against whirling disease have been inconsistent and the drug is not approved for use in food fish in many jurisdictions. Antiparasitic bath treatments effective against external parasites do not reach the internal cartilage locations where Myxobolus cerebralis resides. The focus must therefore be on supportive care rather than curative treatment.

Hospital or quarantine tank setup for whirling disease cases serves primarily to isolate affected fish and prevent disease spread rather than facilitate treatment. Infected fish should be maintained in closed systems where water cannot escape to contaminate other populations. Tanks should have smooth surfaces without gravel or sediment that could harbor tubifex worms or accumulate spores. Removing infected fish from ponds or systems containing tubifex worms prevents ongoing exposure and may allow less severely affected individuals to survive. Hospital tanks should be maintained at the cooler end of the appropriate temperature range and positioned to minimize disturbance that triggers spinning episodes.

Supportive care for whirling disease focuses on minimizing stress and providing optimal conditions for fish that may recover partial function. Reducing water current allows affected fish to maintain position without exhausting themselves fighting flow. Offering highly palatable, easily captured food helps fish with feeding impairment maintain nutrition. Some affected fish can learn compensatory swimming strategies if given a low-stress environment during recovery. Ensuring protection from aggressive tankmates prevents additional stress and injury. While severely affected fish may not survive, those with milder infections can sometimes stabilize and live relatively normal lives despite some permanent deformity.

Treatment duration and monitoring for whirling disease cases involves long-term observation rather than a defined treatment course. Fish should be monitored for weeks to months to assess whether their condition stabilizes or continues to deteriorate. Regular assessment of feeding behavior, swimming ability, and physical condition helps determine prognosis for individual fish. Those showing progressive decline despite supportive care may require humane euthanasia to prevent suffering. Fish that stabilize should continue to be housed separately as they remain carriers capable of releasing spores. Monitoring water and sediment from systems housing infected fish helps assess ongoing contamination levels.

The impact of whirling disease on biological filtration differs from most fish diseases because the organism is not bacterial and standard treatments are not applicable. However, if antiparasitic medications are attempted, their effects on biofilter bacteria should be considered. More importantly, systems that have housed infected fish become contaminated with spores that can persist for decades. Biofilter media, substrate, and all equipment become potential sources of infection. Complete decontamination requires either extended drying periods of several months or treatment with chlorine or calcium hydroxide solutions at concentrations that destroy beneficial bacteria. Essentially, systems exposed to whirling disease may need complete teardown and disinfection to eliminate contamination.

Recovery timeline for whirling disease depends on infection severity, with outcomes ranging from complete mortality in severe cases to survival with permanent deficits in milder infections. Fish that survive the acute phase when parasite multiplication is most active may stabilize over a period of weeks to months. Skeletal deformities that develop during active infection are permanent, as damaged cartilage cannot regenerate and bone formation proceeds based on whatever template remains. Some neurological function may improve as fish develop compensatory strategies, but balance and coordination deficits from inner ear damage typically persist. Young fish infected before significant skeletal development face the poorest prognosis, while older fish with more ossified skeletons may escape with minimal lasting effects.

Post-treatment care and monitoring for whirling disease survivors focuses on ongoing supportive management and containment. Recovered fish remain permanently infected carriers and should never be released to wild waters or mixed with uninfected populations. Monitoring should continue for signs of secondary infections, as the stress of disease and any physical deformities create vulnerability to opportunistic pathogens. Feeding may need to continue with easily captured food items if jaw or swimming deformities impair normal feeding. Regular assessment of body condition helps identify fish that are failing to thrive despite apparent stabilization. Careful biosecurity must be maintained throughout the fish's life to prevent spore release to uncontaminated systems.

Prognosis factors for whirling disease recovery include age at infection, infection intensity, and the specific tissues affected by parasite development. Fish infected as older juveniles with largely ossified skeletons typically have better outcomes than fry infected during early cartilage development. Lower infection intensities result in less tissue destruction and fewer parasites to fuel ongoing damage. Fish with cartilage damage limited to less critical areas may maintain relatively normal function, while those with extensive inner ear or spinal involvement face severe permanent impairment. Species also varies in susceptibility, with rainbow trout generally showing higher mortality than brown trout or brook trout infected under similar conditions.

Return to main tank considerations for whirling disease survivors are primarily governed by biosecurity rather than recovery status. Under no circumstances should fish that have been infected with whirling disease be returned to systems housing uninfected fish, regardless of how well they appear to have recovered. Survivors continue to harbor and release myxospores that can contaminate any system they enter. If survivors are to be maintained long-term, they must remain in dedicated quarantine systems designed to prevent any water or waste from reaching uncontaminated areas. In most hatchery and management contexts, infected populations are culled and facilities decontaminated rather than attempting to maintain carrier fish. For pet fish, long-term isolation in contained systems may be an option if owners choose to provide ongoing care.

Water quality maintenance for whirling disease prevention focuses on reducing conditions favorable to the tubifex worm intermediate host rather than standard water chemistry parameters. Minimizing organic matter accumulation in substrate and sediment reduces tubifex habitat. Maintaining concrete or liner-based raceways rather than earthen ponds eliminates the substrate environment tubifex worms require. Regular cleaning to remove accumulated detritus prevents tubifex population establishment. While excellent general water quality supports fish health and disease resistance, the unique two-host life cycle of Myxobolus cerebralis means environmental management targeting the worm host is equally important. Using well water or treated municipal water rather than surface water from potentially contaminated watersheds eliminates a major exposure route.

Quarantine protocols for new fish represent one of the most critical prevention measures for whirling disease. All fish from any source should be quarantined for a minimum of sixty days before introduction to main populations, as this allows time for symptoms to develop in incubating infections. Purchasing fish only from certified disease-free sources significantly reduces risk, though certification programs vary in rigor between jurisdictions. Testing quarantined fish using PCR methods can detect infections before spore release begins. Any fish showing suspicious signs during quarantine should be tested and the entire quarantine group held until results are available. Quarantine systems must be completely isolated with no water, equipment, or personnel movement to main fish populations.

Nutritional prevention, while not directly effective against the parasite, supports overall fish health and disease resistance. Providing complete, high-quality nutrition ensures fish have optimal immune function and the metabolic resources to mount defense responses. Adequate vitamin C supports connective tissue health and may improve outcomes in fish exposed to cartilage-damaging pathogens. Avoiding overfeeding prevents excess organic matter accumulation that could support tubifex populations. Proper nutrition also supports rapid growth through the vulnerable early life stages when fish are most susceptible, though this must be balanced against temperature and other factors affecting disease progression.

Stress reduction is essential for preventing whirling disease and optimizing outcomes in fish that become exposed. Chronic stress suppresses immune function, increasing both susceptibility to initial infection and severity of disease progression. Minimizing handling, maintaining appropriate stocking densities, providing adequate shelter and environmental complexity, and ensuring stable water conditions all reduce stress. Avoiding sudden temperature changes is particularly important as thermal stress dramatically increases susceptibility to myxozoan parasites. Reducing competition for food through adequate feeding ensures all fish receive nutrition without the stress of aggressive interactions.

Tank maintenance routines and facility biosecurity form the foundation of whirling disease prevention programs. Regular disinfection protocols for equipment, nets, boots, and vehicles prevent mechanical transmission of spores between water bodies. Complete drying of equipment between uses kills most parasites and intermediate hosts. Implementing traffic flow patterns that move from clean areas to potentially contaminated areas, never the reverse, reduces cross-contamination risk. Eliminating any potential for bird access prevents avian predators from transporting infected fish or spores between locations. Maintaining detailed records of fish sources, movements, and any disease events supports traceback investigation and response if disease is detected.

Ongoing tank management for facilities in areas where whirling disease is endemic requires constant vigilance and adherence to biosecurity protocols. Operating with the assumption that the disease could be introduced at any time means maintaining prevention measures even when no cases have been detected. Regular surveillance testing of fish populations provides early warning of any introduction. Monitoring for tubifex worm presence through substrate sampling allows assessment of transmission risk. Maintaining relationships with regulatory agencies and disease diagnostic laboratories ensures rapid response capability if suspicious cases arise. Long-term management plans should include contingencies for responding to disease introduction, including potential depopulation and facility decontamination protocols.

Water change and filtration management in facilities at risk for whirling disease must balance fish health needs against disease transmission potential. Incoming water from surface sources in endemic areas may contain triactinomyxon spores, necessitating treatment through UV sterilization, ozone treatment, or fine filtration before contacting fish. Effluent water containing spores from infected fish poses contamination risk to receiving waters and may require treatment before discharge depending on regulatory requirements. Recirculating systems must be designed to prevent tubifex worm establishment while maintaining biological filtration function. Sand filters and settling basins can become worm habitat and may need regular inspection and treatment.

Monitoring fish health in the context of whirling disease prevention involves regular observation for early warning signs and systematic testing protocols. Daily observation of feeding behavior, swimming patterns, and physical condition allows early detection of problems. Any fish showing neurological signs, skeletal abnormalities, or black tail coloration should be immediately isolated and submitted for testing. Routine surveillance testing of apparently healthy fish provides confidence that disease has not been introduced subclinically. Keeping detailed records of all observations, test results, and fish movements supports epidemiological investigation if disease is detected. Training all personnel in recognition of whirling disease signs ensures comprehensive monitoring coverage.

Compatible tankmate considerations for whirling disease management primarily involve species susceptibility differences. While Myxobolus cerebralis primarily affects salmonids, maintaining other fish species in the same facility creates biosecurity challenges as equipment and water can transfer contamination. Non-salmonid species are not susceptible to disease but could potentially transport spores on their bodies or in gut contents if they consume infected material. Within salmonids, species vary considerably in susceptibility, with rainbow trout showing highest mortality rates, while brown trout, brook trout, and some Pacific salmon species demonstrate relative resistance. Understanding these differences can inform stocking decisions in endemic areas, though resistant species can still become infected carriers.

Long-term care considerations for managing whirling disease risk include planning for climate change impacts on disease dynamics and maintaining institutional knowledge of prevention protocols. Warming water temperatures may expand the geographic range of the disease and alter transmission timing. Succession planning ensures that biosecurity knowledge transfers between personnel over time. Investment in infrastructure such as pathogen-free water supplies, concrete raceways, and UV treatment systems represents long-term commitment to prevention. Engagement with research programs investigating potential treatments, resistant fish strains, and biological control of tubifex worms may provide future management options. Participation in regional disease management cooperatives allows coordinated response to protect shared water resources.

High-risk species for whirling disease are predominantly salmonids, with rainbow trout showing the highest susceptibility and mortality rates among commonly cultured species. Rainbow trout fry infected at young ages can experience mortality rates exceeding ninety percent, and survivors typically display severe deformities. Brown trout demonstrate moderate susceptibility with lower mortality rates, though they can still become infected carriers that perpetuate the disease cycle. Brook trout and various Pacific salmon species including chinook and coho show variable susceptibility depending on age at exposure and environmental conditions. Cutthroat trout, particularly the Yellowstone cutthroat subspecies, have shown significant vulnerability in wild populations where the disease has become established. The sockeye salmon appears relatively resistant but can still harbor infections.

Freshwater considerations for whirling disease center on the fact that this is exclusively a freshwater disease affecting fish during their freshwater life stages. The tubifex worm intermediate host requires freshwater habitat, limiting disease transmission to rivers, streams, lakes, ponds, and freshwater aquaculture facilities. Salmon species that spend portions of their life cycle in marine environments only face infection risk during freshwater phases, providing some protection to anadromous populations that quickly migrate to sea. However, hatchery-reared salmon held in freshwater for extended periods face the same risks as resident freshwater species. Stocking programs that raise fish to larger sizes before release may inadvertently increase exposure time during vulnerable periods.

Species-specific susceptibilities within the salmonid family relate to differences in cartilage composition, immune responses, and potentially genetic factors that remain incompletely understood. Young fish with abundant actively growing cartilage face the highest risk regardless of species, as the parasite specifically targets these tissues. Species demonstrating some resistance may possess cartilage structural differences that impede parasite penetration or development, though research continues to investigate the mechanisms involved. Selective breeding programs have identified family lines within rainbow trout showing improved survival following infection, suggesting genetic resistance exists and could potentially be enhanced through selective breeding. Wild populations that have coexisted with the disease for extended periods may have evolved some level of natural resistance through selection pressure, though this adaptation comes at the cost of population declines during the selection process.

Commonly co-occurring conditions with whirling disease primarily involve secondary infections that take advantage of the weakened and stressed state of affected fish. Bacterial infections including furunculosis, enteric redmouth disease, and bacterial gill disease frequently develop in fish compromised by whirling disease. Fungal infections often colonize damaged tissue or affect fish with impaired immunity. The stress of disease and resulting immunosuppression creates vulnerability to opportunistic pathogens that healthy fish would normally resist. Additionally, the physical deformities caused by whirling disease can lead to chronic secondary problems such as scoliosis-related organ compression or respiratory compromise from opercular malformation that create ongoing health challenges beyond the primary parasitic infection.

Conditions with similar symptoms to whirling disease include other neurological diseases of fish that cause spiral swimming or loss of equilibrium. Viral hemorrhagic septicemia can produce spiral swimming and darkened coloration but typically presents with hemorrhaging not seen in whirling disease. Infectious hematopoietic necrosis causes similar neurological signs in salmonid fry along with abdominal distension and hemorrhage. Nutritional deficiencies, particularly of tryptophan, can cause scoliosis resembling whirling disease deformities but without the progressive neurological deterioration. Vertebral compression fractures from handling trauma or nutritional problems create spinal deformities that may superficially resemble whirling disease but develop acutely rather than progressively. Other myxozoan parasites occasionally cause neurological disease in fish with different species specificity and geographic distribution.

Secondary infections and complications following whirling disease reflect both direct tissue damage and the immunosuppressive effects of chronic parasitic infection. Skeletal deformities can lead to chronic pain, abnormal organ positioning, and impaired function of compressed internal organs. Fish with jaw deformities may develop chronic malnutrition due to inability to feed effectively. Opercular deformities expose delicate gill tissue to damage and infection while compromising respiratory efficiency. The ongoing stress of living with disability and the metabolic burden of chronic infection leave fish vulnerable to any additional health challenges. In wild populations, the inability to escape predators or compete effectively for resources leads to high post-recovery mortality even among fish that survive the acute infection phase.