What is Hirsutella thompsonii and why is it used as a mycoacaricide?

Hirsutella thompsonii Fisher is a fungus that naturally infects and kills mites. "Mycoacaricide" simply means a mite-control product based on a fungus. It is used because it is one of the few fungal pathogens whose natural hosts are plant-feeding mites rather than insects, because it causes natural population crashes in eriophyid mites in the field, and because it has a mode of action unrelated to synthetic acaricides. It belongs to the Ascomycota, family Ophiocordycipitaceae [11].

Does Hirsutella thompsonii control coconut eriophyid mite (Aceria guerreronis)?

Coconut mite is one of the best-documented targets. In a field study in India, a mycelial formulation of H. thompsonii tank-mixed with adjuvants reduced post-treatment coconut mite populations by 85.6–97.1%. Palms treated with the fungus plus glycerol showed a mean pre-harvest nut damage grade of 2.0, against 4.0 in untreated control palms [1].

Two boundaries on that result. It was obtained with a specific mycelial formulation and specific adjuvants, and coconut mite lives under the fruit perianth, which makes spray coverage the limiting factor in practice. Results depend heavily on getting inoculum into that sheltered space.

How does Hirsutella thompsonii infect and kill mites?

By direct penetration of the cuticle, followed by internal colonization — not by ingestion, and not by contact paralysis.

Scanning electron microscopy of the infection sequence on Brevipalpus phoenicis showed conidia attached to the mite integument within 24 hours, germinating and penetrating at the base of the setae on the hysterosoma; colonization was evident by 48 hours, and mycelium and conidiophores emerged from the cadaver by 120 hours [6]. On Varroa destructor, the point of entry was identified as the membranous arolium of the leg sucker [7].

The fungus also produces hirsutellin A (HtA), a 15 kDa protein toxin [2] that has been characterized as a ribotoxin — it inactivates ribosomes by cleaving a single specific bond in ribosomal RNA, shutting down protein synthesis in the host [3][4]. Purified HtA reached close to 100% mortality of adult citrus rust mite at 100 µg/mL in leaf bioassays, and reduced egg-laying before the mites died [9].

Importantly, the toxin is not the whole story. A survey of 162 H. thompsonii strains found the HtA gene in 100 of them, but its presence was not associated with greater insecticidal activity — strains with and without an amplifiable HtA gene produced filtrates causing the same average mortality. The authors concluded that HtA is required for neither survival nor pathogenicity, and that other, uncharacterized factors are involved [5]. A separate study found that an exudate from sporulating cultures suppressed spider mite egg-laying through a factor distinct from HtA [8].

Which types of mites are most commonly targeted by Hirsutella thompsonii?

Chiefly three families:

• Eriophyidae (rust, bud, gall and blister mites) — citrus rust mite, coconut mite, rubber tree mites. This is where the evidence is strongest [1][9][12]

• Tenuipalpidae (false spider mites) — Brevipalpus phoenicis, where H. thompsonii was by far the most virulent of 52 fungal isolates screened [6]

• Tetranychidae (spider mites) — effects on Tetranychus urticae are documented, including strong suppression of egg-laying [8]

It has also been studied against the honey bee parasite Varroa destructor [7][13]. It is not universally pathogenic to mites: against the scab mite Psoroptes ovis it showed no pathogenicity in laboratory testing [14].

Why do humidity, temperature and sunlight affect Hirsutella thompsonii performance?

Because every step of infection is a biological process happening on an exposed leaf or fruit surface.

Humidity is the critical one. A conidium must take up water to germinate before it can penetrate the mite. This requirement is well enough established to have decided the outcome of a commercial program: in Israel, H. thompsonii was introduced twice against citrus rust mite and killed 80–90% of exposed mites, but "due to its requirements for near-saturation humidities was deemed unsuitable for local outdoors conditions" [10]. That is the single most important limitation of this organism, and any honest recommendation has to start there.

Sunlight damages fungal propagules and reduces the fungus's ability to produce new spores. Irradiance with simulated sunlight reduced conidiogenesis in laboratory work, although adjuvant treatment substantially offset the loss [1].

Temperature governs the speed of germination and growth. It interacts with humidity: warm dry conditions are the worst combination, because they accelerate drying of the spray deposit without supporting infection.

The seasonal pattern in the field follows directly. In Brazilian rubber plantations, natural infection of pest mites peaked from November to February — the rainy season — and fell below 5% in the dry season [12].

What is the best time of day or weather condition to apply Hirsutella thompsonii?

Early morning or late afternoon, into a humid period, with rain not imminent.

• Late afternoon application gives the deposit a full night of high humidity and dew before the next day's sun

• Early morning application also works where dew persists

• Avoid mid-day application in bright sun and low humidity

• Avoid spraying immediately before heavy rain, which washes inoculum off before it establishes

• In monsoon-influenced systems, applications before the onset of monsoon and after monsoon are the conventional pattern for perennial crops

• Prefer overcast, humid conditions over clear, dry ones

Time of day matters, but it is second to humidity. A perfectly timed evening spray into a dry spell will still underperform.

Can Hirsutella thompsonii be mixed with fungicides, acaricides or other crop-protection products?

Treat fungicides as incompatible unless a specific test says otherwise. H. thompsonii is a fungus. A fungicide that controls plant pathogens will generally also affect it, and this is the most common way a biological acaricide application is wasted.

For other products, published compatibility data specific to H. thompsonii is limited, and general findings from related fungi do not transfer reliably. In one study of acaropathogenic fungi in Israel, three species tolerated most locally used insecticides and acaricides with the notable exception of sulfur [10] — but that result was for Meira and Acaromyces species, not for H. thompsonii, and should not be read across.

The honest position: compatibility should be confirmed under the intended tank-mix conditions before commercial use. Evaluate physical mixing, viability of the fungus after the expected contact period, plant safety and performance. Where a mix has not been tested, apply the products separately and leave an interval between them.

The current product documentation states compatibility with biopesticides, biofertilizers and plant growth regulators, and incompatibility with chemical fertilizers and chemical pesticides. Follow that guidance and verify locally before scaling a new mix.

Does Hirsutella thompsonii affect beneficial insects or predatory mites?

The evidence separates into two parts, and the second is often left out.

Beneficial insects. In honey bee studies, H. thompsonii was harmless to the bees at the concentrations applied and had no deleterious effect on queen fecundity [13]. A separate study found it did not infect honey bees at larval, prepupal, pupal or adult stages under the rearing conditions used [7].

Predatory mites. Here there is a measurable effect. A formulated H. thompsonii product tested against the predatory mite Phytoseiulus longipes significantly reduced its net reproductive rate, intrinsic rate of increase and finite rate of increase. Under the IOBC toxicity classification the product was rated slightly harmful to adults, and residues became harmless to the predator around 10 days after spraying [16]. For comparison, in the same study four conventional insecticides were highly harmful to both eggs and adults and remained so past 31 days.

The practical reading: H. thompsonii is markedly gentler on predatory mites than broad-spectrum chemistry, but it is not inert toward them. Where predatory mites are released as part of the program, allow roughly 10 days between application and release.

Why can field performance of Hirsutella thompsonii vary between crops and seasons?

Six reasons, most of which can be managed:

• Humidity and season. The dominant factor. Natural infection rates in one field system ranged from a rainy-season peak to under 5% in the dry season [12], and a whole commercial program was judged unsuitable in one region because the local climate did not supply the humidity the fungus needs [10]

• Mite species. Susceptibility differs by family and by species, from highly susceptible eriophyids and tenuipalpids through to species that showed no infection at all [6][14]

• Strain. Only three of nine isolates were infectious in one screen, and speed of kill varied nearly two-fold among those three [7]

• Coverage and mite habitat. A mite sheltered under a coconut perianth or on the underside of a dense canopy is much harder to reach than one on an exposed fruit surface

• Sunlight and formulation. Solar exposure reduces spore production, and adjuvants measurably offset that loss — one adjuvant raised conidium density by an average of 106% over control and boosted pathogenicity by 16.5% [1]

• Crop microclimate and surroundings. Management type and adjacent native vegetation both influenced infection rates in rubber plantations, with native vegetation acting as a reservoir and moderating the crop microclimate [11]

The implication for a grower is that this product rewards attention to conditions. Applied into humid weather, at the right mite stage, with full coverage of the infested plant part, it performs very differently from the same product applied into a dry, sunny window.