Sweating sickness is an acute, febrile, tickborne toxicosis characterized mainly by a profuse, moist eczema and hyperemia of the skin and visible mucous membranes. It is essentially a disease of young calves, although adult cattle are also susceptible. Sheep, pigs, goats, and a dog have been infected experimentally. It occurs in eastern, central, and southern Africa and probably in Sri Lanka and southern India.
The cause of sweating sickness is an epitheliotropic toxin produced by females of certain strains of Hyalomma truncatum. The toxin develops in the tick, not in the vertebrate host. Four tick salivary gland proteins with molecular mass ranging from 27–33 kDA have been proposed to be associated with sweating sickness immunodominance, whereas a 32 kDA band salivary gland protein was found to be unique to a sweating sickness–positive strain. The potential to produce toxin is retained by ticks for as long as 20 generations, and possibly longer. Attempted experimental transmissions between affected and healthy animals by contact or inoculations of blood have been unsuccessful.
Graded periods of infestation of a susceptible host by “infected” ticks have different effects on the host. A very short period has no effect; the animal remains susceptible. A period just long enough to produce a reaction may confer immunity, but if the exposure is >5 days, severe clinical signs and death may result. Recovery confers a durable immunity, which may last ≥4 yr. Other closely related forms of H truncatum toxicoses have been described.
After an incubation period of 4–11 days, signs appear suddenly and include hyperthermia, anorexia, listlessness, watering of the eyes and nose, hyperemia of the visible mucous membranes, salivation, necrosis of the oral mucosa, and hyperesthesia. Later, the eyelids stick together. The skin feels hot, and a moist dermatitis soon develops, starting from the base of the ears, the axillae, groin, and perineum and extending over the entire body. The hair becomes matted, and beads of moisture may be seen on it. The skin becomes extremely sensitive and emits a sour odor. Later, the hair and epidermis can be readily pulled off, exposing red, raw wounds. The tips of the ears and the tail may slough. Eventually, the skin becomes hard and cracked and predisposed to secondary infection or screwworm infestation. Affected animals are sensitive to handling, show pain when moving, and seek shade.
Often, the course is rapid, and death may occur within a few days. In less acute cases, the course is more protracted and recovery may occur. Mortality in affected calves is 30%–70% under natural conditions. Morbidity in endemic areas is ~10%. The severity of infection is influenced by the number of ticks as well as by the length of time they remain on the host.
Emaciation, dehydration, diphtheroid stomatitis, pharyngitis, laryngitis, esophagitis, vaginitis or posthitis, edema and hyperemia of the lungs, atrophy of the spleen, and congestion of the liver, kidneys, and meninges are found, in addition to the skin lesions. Experimentally infected adult cattle showed typical lesions of moist eczema, and mucous membrane changes were accompanied by a marked decrease in circulating leukocytes with severe neutropenia.
For diagnosis, it is essential to determine the presence of the vector. Typically, there is a generalized hyperemia with subsequent desquamation of the superficial layers of the mucous membranes of the upper respiratory, GI, and external genital tracts, and profuse moist dermatitis followed by superficial desquamation of the skin.
Control of tick infestation is the only effective preventive measure. Adult ticks show a predilection to attach in the tail switch. Removal of ticks, symptomatic treatment, and good nursing care are indicated. Non-nephrotoxic antibiotics and anti-inflammatory agents are useful to combat secondary infection. Immune serum can be an effective specific treatment, although associated with problems of donor availability, possible serum contamination, and IV administration of a relatively large volume. A refined precipitated immunoglobulin suspension proved ineffective as a specific treatment, probably because of low concentrations of effective immunoglobulins.