Xenohaliotis Californiensis: How It Affects On Abalone

Xenohaliotis Californiensis is a disease which affects abalone, often causing large scale mortalities. This article, from the OIE, looks at the causes of the disease, its life cycle and advise if the disease is present in stocks.


Intracytoplasmic infections with Xenohaliotis californiensis, a rickettsial bacterium, in gastrointestinal epithelia causes disease (termed withering syndrome) in wild and farmed abalones, Haliotis spp. (Vetigastropoda: Mollusca). Gross signs of the disease include pedal atrophy, mottled digestive gland, anorexia, weakness, and lethargy.

Disease information

Agent factors

Aetiological agent, agent strains

Xenohaliotis californiensis is an intracellular bacterium in the family Anaplasmatacea and is closely related to members of the genera Ehrlichia, Anaplasma and Cowdria. The disease caused by this bacterium is known as withering syndrome and may be more appropriately termed abalone rickettsiosis. No information exists on the presence of strain variations of this bacterium. The dimorphic rod-to-spherical-shaped bacterium measures an average of 332 × 1550 nm in the bacillus form and an average of 1405 nm in the spherical morphotype. The bacterium reproduces within intracytoplasmic vacuoles 14–56 µm in diameter within gastrointestinal epithelia.

Survival outside the host

Although X. californiensis is thought to be an obligate intracellular organism, the bacterium may survive outside the host for an undetermined period of time as evidenced by water-borne transmission studies.

Stability of the agent (effective inactivation methods)

Based on successful decontamination in the laboratory, this bacterium is readily inactivated by immersion in <10 per cent bleach. In addition, exposure of seawater containing the bacterium to >10 mg litre–1 [ppm] calcium hypochlorite and disinfection of equipment in a bath of 1 per cent tamed iodine in freshwater for 1 hour are effective disinfectants based on the use of these disinfection methods at a marine laboratory with flow- through seawater and a lack of detection of this pathogen in adjacent abalone populations.

Life cycle

The bacterium divides by binary fission and has direct, horizontal transmission. Although not typically observed in farmed abalones until they are in grow-out conditions (>2.5 cm maximum size), polymerase chain reaction (PCR) examination of exposed 6-week-old abalones suggested that 1–2 mm abalones may become infected (Moore et al., unpublished observations).

Host factors

Susceptible host species

Xenohaliotis californiensis infects members of the genus Haliotis and natural infections have been observed in black abalones (H.cracherodii), white abalones (H. sorenseni), red abalones (H. rufescens), pink abalones (H. corrugata), green abalones (H. fulgens), the small abalone (H. diversicolor supertexta), the European abalone in the wild or culture facilities, as well as flat (H. wallalensis) and Japanese abalones (H. discus-hannai) in laboratory challenges (Friedman, unpublished observations). Other abalone species have not been tested.

Susceptible stages of the host

While all post-larval life stages have been demonstrated susceptible to infection with X. californiensis, clinical disease is typically observed in animals >1 years of age in farmed abalones (Friedman, unpublished observations) and all abalone size classes observed in wild populations surveyed to date.

Species or subpopulation predilection (probability of detection)

Probability of detection increases with increasing abalone size. Animals less than 10 mm in size have a reduced probability of detection using histology but equal probability of detection using PCR.

Target organs and infected tissue

Xenohaliotis californiensis infects the gastrointestinal epithelial cells of the posterior oesophagus, digestive gland and, to a lesser extent, intestine.

Persistent infection with lifelong carriers

Infections may persist for long periods without the development of clinical disease when the host is maintained at cool water temperatures (e.g. 15°C for red abalones), and exposure to elevated seawater temperatures (e.g. >17°C for red, black and white abalones) typically results in clinical disease. Recent data suggest that some species, especially those inhabiting warmer waters may harbour the bacterium without the development of clinical disease.


Although no alternate, non-haliotid hosts have been identified, it has been suggested that some colonial ascidians may concentrate the bacterium (based on PCR evidence). Thus, the possibility of such species acting as a vector for the bacterium exists, but further investigation of possible vectors are warranted.

Known or suspected wild aquatic animal carriers


Disease pattern

Disease (withering syndrome) occurs at elevated water temperatures (~18°C and above) in abalones with moderate to severe infections. The incubation period of withering syndrome is prolonged and typically ranges between 3 and 7 months. Clinical disease is characterised by morphological changes in the digestive gland, which vary between species and may include degeneration (atrophy of tubules, increase in connective tissues and inflammation) and/or metaplasia of the digestive tubules. Metaplasia involves the replacement of terminal secretory/absorptive acini with absorptive/transport ducts similar in appearance to the post-oesophagus. These morphological changes are accompanied by anorexia, depletion of glycogen reserves, followed by use of the foot muscle as an energy source and subsequent death. The foot of affected abalones contain fewer and less organised muscle bundles, abundant connective tissue and may contain more cerous cells than unaffected individuals. Surviving abalones appear to remain infected, even in low water temperature environments, such as in northern California.

Transmission mechanisms

Transmission of X. californiensis is horizontal and is postulated to be via a faecal–oral route. Exposure of abalones to seawater containing infectious material is sufficient for transmission of the bacterium, and no direct animal contact is required. Temperatures below 13°C have been demonstrated to limit transmission of the bacterium (i.e. less than 1 per cent transmission) relative to those held at ~18°C (72– 94 per cent transmission).

Table Prevalence Table 2.1. Variation in the prevalence of Xenohaliotis californiensis among species and location
Species PCR prevalence Histology prevalence References
  Wild Farmed Wild Farmed  
Haliotis rufescens ND 0–100% 1–75%1 0–100%2 8, 16, Friedman, unpublished obs.
Haliotis cracherodii ND NA 74–98% NA 8
Haliotis sorenseni 0 0–100% 0 0–100% 11, Moore et al., unpublished obs.
Haliotis fulgens ND ND 44–100% ND 21
Haliotis corrugata ND ND 62–63% ND 21
Haliotis walallensis NA NA 0 NA J.D. Moore, unpublished obs.
Haliotis discus-hannai ND 0 0 0 C.S. Friedman, unpublished obs.
Haliotis diversicolor supertexta ND 61% ND 53% 233
Haliotis tuberculata         3
1Prevalences of 1–17% have been observed in northern California and up to 75% in central and southern California.
2Larger abalones typically have a higher prevalence of infection.
3Only 36 animals were sampled from one farm in Thailand. ND = no data: NA = not applicable.

Geographical distribution

Xenohaliotis californiensis occurs along the south-west coast of North America in California, USA and Baja California, Mexico. However, as infected abalones have been transported to Chile, China (People’s Rep. of), Chinese Taipei, Iceland, Ireland, Israel, Japan, Spain, and Thailand and possibly other countries, the geographical range of the aetiological agent is suspected to be broad where California red abalones, Haliotis rufescens, are cultured or areas where native species have been exposed to red abalones.

Mortality and morbidity

Susceptibility varies with species, since the bacterium is known to cause disease in black (up to 99 per cent mortality), white (up to 100 per cent mortality, red (up to 35 per cent mortality), pink (also called yellow) and green (also called blue) abalones. Unlike the other abalone species studied to date, the magnitude of abalone mortality is not well documented in pink and green abalones. However, in Baja California, Mexico, up to 100 per cent of green (blue) and 63 per cent of pink (yellow) abalones may be infected, with up to 43 per cent of the green and 71 per cent of the pink abalones having microscopic signs of disease (degenerated or metaplastic digestive gland). The incubation period varies with temperature but typically involves a prolonged 3–7 month prepatent period. Mortality typically occurs 1–2.5 months after the onset of visible clinical signs. Xenohaliotis californiensis was recently observed, based on histological and molecular data, in several Asian countries including China (People’s Rep. of), Chinese Taipei and Thailand. Prevalence has not been well documented but up to 61 per cent of H. diversicolor supertexta were infected at a farm in Thailand, however, like the European abalone, H. tuberculata, no abalones exhibited clinical signs of withering syndrome.

Environmental factors

Disease (withering syndrome) occurs at elevated water temperatures (~18–25°C in abalones with moderate to severe infections. Parasite transmission is enhanced in fed (94 per cent) as opposed to starved (72 per cent) abalones. Subclinical infections have been observed in H. diversicolor supertexta raised at 27–29°C. As abalones are obligate marine species, salinity tolerances of the Rickettsia-like organism (RLO) have not been investigated.

Control and prevention

The most effective prevention is avoidance of the pathogen. Should infection occur, holding abalones at <15°C may reduce RLO transmission and subsequent disease transmission (4). Application of oxytetracycline reduces losses.


Vaccination is not a viable option in controlling infection with X. californiensis.


Reducing densities and application of an oxytetracycline-medicated diet may reduce losses. Oral administration of 12–19 per cent TM-100 (90–100 mg kg–1) in a medicated diet for 10 or 20 days provides protection against bacterial re-infection for several months. Recent data suggest that a single day oral administration of 12 per cent TM-100 can reduce bacterial infections from 80 per cent to 10 per cent prevalence and mean infection intensity from 1.4 to 0.1 on a scale of 0–3. Based on the observation of oxytetracycline in unmedicated abalones that received seawater from treated animals, it is thought that either intake of seawater containing the drug or absorption may be the key route of uptake for this therapeutant.


No data exists on immunostimulation as a control measure for this disease.

Resistance breeding

Interest in selecting for resistant abalones, particularly for restoration purposes, is increasing. Wild black abalones are recruiting along the California Channel Islands and some recruits survive, suggesting that these individuals may be more resistant to this rickettsial disease (VanBlaricom, pers. obs.). Recent laboratory trials have demonstrated enhanced disease resistance in progeny of black abalones that survived X. californiensis relative to those from non-disease selected populations (Friedman et al. unpublished data).

Restocking with resistant species

No data currently exists and one must consider the relative merits of culturing alternate species.

Blocking agents

No data.

Disinfection of eggs and larvae

No attempts to disinfect eggs and larvae have been undertaken. Abalone larvae are non-feeding and it is unlikely that transmission occurs prior to settlement and metamorphosis after which feeding begins (Moore & Friedman, unpublished data).

General husbandry practices

Husbandry practices to reduce problems caused by X. californiensis are typical of those for any bacterial disease and include the purchase of inspected seed (devoid of evidence of infection), maintaining separate families or groups (i.e. avoid high grading and mixing of disparate groups), rinsing hands and equipment in freshwater or iodinated water and drying them in between uses. Isolation of infected groups is recommended if possible. If oxytetracycline treatment is employed, therapeutic application under federal guidelines (e.g. FDA-CVM1 in the USA or EMEA2 in Europe) prior to the warm water season may reduce losses and infection. Typically, only a single application during the second or third year of growth is required during a typical 3–4 year culture cycle.

March 2011

the Fish Site Editor

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