Sweet potato phoma rot

The fungus survives in soil and crop debris through the formation of pycnidia, which are specialized black fruiting bodies containing fungal spores. These structures allow the pathogen to remain viable in the soil for several years.

Disease development is highly dependent on environmental moisture. Spores are released from pycnidia and spread through splashing rain, irrigation water, or contaminated tools to infect healthy plant tissues.

Once infection is established, the mycelium penetrates deep into the tissues, causing cell death and necrosis. The fungus spreads systematically within the plant, eventually producing new pycnidia on the surface of the lesions.

The spread of the disease is predominantly facilitated by the movement of infected plant material (slips and tubers) and contaminated soil, making phytosanitary control at the source a priority.

The primary host for Plenodomus destruens is the sweet potato (Ipomoea batatas). The disease affects both the vegetative parts and the root storage organs, causing significant economic losses.

In the field, infection at the stem base can cause severe wilting and plant death. Young plants are particularly vulnerable, and systemic infection can lead to complete failure of the stand if left unmanaged.

The most critical damage occurs on the storage roots (tubers). Phoma rot makes tubers unmarketable and unsuitable for processing, often appearing after harvest during storage periods.

In storage environments, the pathogen can spread from infected tubers to healthy ones through direct contact. This can result in the loss of a high percentage of the stored harvest in a relatively short time.

The economic impact is two-fold: direct reduction of sellable volume and increased costs associated with crop destruction and loss of planting material for the next season.

The first symptoms on stems appear as dark, slightly depressed spots around the soil line. As the infection progresses, the stem tissue turns brown and brittle, leading to the collapse of the vine.

On tubers, the symptoms manifest as brown, circular, sunken lesions. As the lesion enlarges, the underlying tissue dries out, becomes corky, and turns dark, which is typical of dry rot symptoms.

A diagnostic sign is the presence of numerous tiny, black, pimple-like pycnidia breaking through the skin of the lesions on both stems and tubers. These can be clearly seen with the naked eye or a hand lens.

When an infected tuber is cut open, the affected area shows a distinct brown discoloration. The diseased tissue is dry and firm, contrasting with the soft, mushy tissues associated with other types of storage rots.

In storage conditions with poor ventilation, the surface of the lesions may show a faint grayish mycelial growth. Severely affected tubers become shriveled, mummified, and light in weight.

The cornerstone of management is the use of disease-free planting material. Growers should source slips only from certified, pathogen-free environments to prevent the introduction of the fungus to new fields.

Strict crop rotation is essential to break the pathogen's life cycle. Avoiding sweet potato cultivation in the same field for at least 3 to 4 years allows the soil-borne inoculum levels to decline significantly.

Sanitation practices play a vital role. This includes the complete removal and destruction of crop residues after harvest and the control of host weeds in and around the production area.

Storage management should prioritize maintaining cool, dry conditions and good airflow. Regularly inspecting stored tubers and removing any that show symptoms of decay is critical to preventing the spread of the infection.

Handling practices that minimize tuber bruising and injury during harvest and sorting are highly effective, as the fungus primarily enters through physical wounds. Chemical seed treatment may be used as a supplementary measure in areas with high disease pressure.