Trypanosoma congolense

Synonyms: Trypanosoma nanum, T. confusum, T. pecorum, T. somaliense, T. cellii, T. frobeniusi, T. montgomeryi, T. ruandae.

Disease: The South African disease of cattle known as nagana is ordinarily caused by T. congolense. Other names which have been given to the disease are paranagana, Gambia fever, ghindi and gobial.

Hosts: Cattle, equids, sheep, goats, camels, dogs and, to a lesser extent, swine. Antelopes, giraffes, zebras, elephants and wart hogs are also infected and act as reservoirs.

Location: This species develops almost exclusively in the blood. It does not invade the lymph or central nervous system.

Geographic Distribution: Widely distributed in tropical Africa between 15 N and 25 S latitude, coinciding with the distribution of the tsetse flies which act ad its vectors.

Prevalence: T. congolense is the commonest and most important trypanosome of cattle in tropical Africa.

Morphology: This species is small, being 8 to 20 u, long; the mean lengths of different populations range from 12.2 to 14.4 u (Hoare, 1959). It lacks a free flagellum or has a short one, has an inconspicuous undulating membrane, and a medium-sized kinetoplast which lies some distance from the posterior end and is typically marginal.

Life Cycle: The vectors of T. congolense are various species of Glossina, including G. morsitans, G. palpalis, G. longipalpis, G. pallidipes and G. austeni. After the trypanosomes have been ingested by the tsetse flies, they develop in the midgut as long trypanosomes without a free flagellum. They then migrate to the proventriculus and thence to the proboscis, where they assume a crithidial form without a free flagellum. These are attached at first to the wall of the proboscis and multiply for a time. Later they pass into the hypopharynx, where they turn into metacyclic, infective trypanosomes similar in appearance to the blood forms. These are injected into the blood stream when the flies bite. T. congolense can also be transmitted mechanically by other biting flies in tsetse-free areas.

Pathogenesis: Many strains which differ markedly in virulence and also in antigenic properties are united under T. congolense (Fiennes, 1950). In cattle, the parasite may cause an acute, fatal disease resulting in death in about 10 weeks, or a chronic condition with recovery in about a year, or a mild, almost asymptomatic condition (Hornby, 1949). The disease is similar in sheep, goats, camels and horses. Swine are more resistant. The signs of trypanosomosis due to this species are similar to those caused by other trypanosomes, except that the central nervous system is not affected.

Fiennes (1953) described the lesions observed in untreated T. congolense infections of cattle. The lymph nodes are edematous, the liver is congested, the marrow of the long bones is largely destroyed, and there are hemorrhages in the heart muscle and renal medulla. In cattle treated with antrycide or dimidium, the lesions are more chronic. The spleen is enlarged, the liver is swollen and sometimes fibrous, the lymph nodes are hypertrophied, edematous and somewhat fibrotic, the kidneys show chronic degeneration, the hemolymph tissue is hyperplastic, and the marrow of the long bones is largely destroyed.

Fiennes (1950), described a cryptic form of trypanosomiasis in cattle, usually following drug prophylaxis or unsuccessful drug therapy, in which severe lesions occur in the heart. These lesions were associated with degenerate or lysed trypanosomes, but some normal forms were also present. This is probably similar to the condition described by Curasson (1943) and Reichenow (1952), in which masses of degenerating trypanosomes plug the capillaries.

Diagnosis: This disease can be diagnosed by detection of the parasites in blood smears. Repeated examinations may be necessary in chronic cases. Inoculation of rats or guinea pigs may give positive results when blood examinations are negative.

Cultivation: Same as for T. brucei.

Treatment: No effective treatment was known for either T. congolense or T. vivax until after World War II. Several drugs have been introduced since then, and active research is still going on. The general pattern has been similar. Each new drug was introduced with glowing accounts of its effectiveness, later its limitations were discovered, and it was either dropped or assumed its place in the trypanocidal armamentarium while the search passed on to a new field. The review articles listed under treatment of T. brucei may be consulted for further information, but progress is being made so rapidly that both they and some of the recommendations below may soon be out of date.

Ethidium is the most effective and safest of several phenanthridinium derivatives which have been used. Cattle are treated by intramuscular injection of 1 mg/kg ethidium bromide or chloride. The trypanosomes disappear from the blood within 2 days. The earlier phenanthridinium compounds caused photosensitization and liver damage, but Ethidium apparently does not.

Antrycide methyl sulfate is also effective against T. congolense. Cattle are treated with a single subcutaneous injection of 4.5 to 5.0 mg/kg, while 3 to 5 mg/kg is used in horses and dogs. Antrycide causes a painful local reaction when given subcutaneously, and may sometimes also cause increased salivation, sweating and tremors. In addition, there are a number of reports of drug-fastness developing to antrycide.

The diamidine, Berenil, has been used with success in preliminary experiments, but has yet to be completely evaluated. The dosage for cattle is about 2 mg/kg subcutaneously or intramuscularly.

The above recommendations deal with curative treatment. A great deal of work has also been done on chemical prophylaxis of trypanosomosis. The idea here is to inject drugs in relatively insoluble form so that they will be released slowly over a long period of time and will protect animals for months.

Antrycide chloride, which is much less soluble than antrycide methyl sulfate, is used for prophylaxis. In actual use, a mixture of 3 parts of the methyl sulfate and 4 of the chloride, known as Antrycide prosalt, is employed. The methyl sulfate eliminates any trypanosomes that might be present at the time of treatment, and the chloride provides the prophylaxis. The prosalt is injected subcutaneously in amount sufficient to give 5 mg/kg of the methyl sulfate. In areas where there are relatively few tsetse flies (defined as an apparent density (AD) of less than 10 flies caught per 10,000 yards of patrol, using a standardized catching technic), treatment every 2 months is effective, but under heavy challenge (defined as an AD of 40 or more) this protection may break down.

Prothidium (R.D. 2801), which contains the pyrimidine moiety of Antrycide linked to a phenanthridinium instead of a quinoline nucleus, was introduced in 1956 as a prophylactic agent. According to Robson and Cawdery (1958), it is better than Antrycide prosalt, a single subcutaneous dose of 4 mg/kg protecting zebus naturally exposed to T. congolense, T. vivax and T. brucei injections for 110 or more days.

Complexes or salts of suramin with Ethidium, Antrycide and other trypanocides were introduced by Williamson and Desowitz (1956) for prophylactic use. They obtained more than 7 months' protection against T. congolense and T. vivax by subcutaneous injection of Ethidium suraminate. However, Robson and Cawdery (1958) considered that the local reactions which it produced were so severe as to preclude its use even tho at 5 mg/kg it protected naturally exposed zebus for 113 days or more. Further work with such complexes may be rewarding.

Pentamidine has been used extensively in prophylaxis of human trypanosomosis, but is not used in domestic animals.

Whenever a drug is used continuously for prophylaxis, there is danger that drug-fast strains of parasites may appear because the blood level becomes so low that relatively resistant individuals can survive. This has happened particularly with Antrycide and also with the phenanthridinium derivatives. Unfortunately, too, strains which have become resistant to Antrycide are also resistant to phenanthridinium compounds. No drug resistance has appeared so far to Berenil.

Control: Same as for T. brucei.