Brill-zinsser disease is recrudescence of epidemic typhus which occurs years after the original disease. Organisms are the same (R. prowazekii). The clinical picture resembles epidemic typhus. The Weil-Felix reaction is negative, but diagnosis is established by complement fixation, microscopic agglutination and immuno fluorescent antibody reactions. Treatment is on same lines as in cases of typhus fever.
Typhus disease is wide spread in India, Asia and Pacific Islands. It also occurs in Japan, South Korea, Nepal, Pakistan and northern Australia. The agent, R tsutsugamushi is transmitted by larvae of several species of mites.
These mites have a four stage life cycle – egg, larva, nymph and adult. The chigger phase is the only stage that is parasitic on animals or humans. These larvae feed on small rodents and man gets infected when approaching a Scrub growth.
Once these chiggers have grasped a host, they attach themselves to the skin where it is thin or wrinkled. These insert their mouth piece towards hair follicles and inject large number of Rickettsiae when it feeds. The organism proliferates in the endothelium of small vessels releasing cytokines which damage endothelial integrity leading to focal occlusive end angitis.
Clinical features of Brill-zinsser disease
The incubation period of disease varies from 5 to 14 days. High body temperature is the most common symptom which begins abruptly with chills, malaise, headache, rigors, post orbital pain, diarrhea and generalized lymphadenopathy. A small papule may appear after 2-3 days of attachment of larva to skin. This soon turns into a necrotic eschar developing into a black slough which separates from the 10th day onwards leaving behind a punched out ulcer. There is regional lymphadenopathy.
Fever in a case of scrub typhus increases progressively during the first week. Initially it is intermittent, remittent or continuous but subsequently becomes continuous and subsides by lysis on the fourteenth to seventeenth day. Despite high temperature, pulse is slow.
By the end of first week there is generalized lymphadenopathy, a red macular rash which began on the trunk by 5th day, spreads to the extremities. Pain in the chest and pneumonitis develops. Patient may go into circulatory collapse myocarditis, nerve deafness, photo-phobia and meningo encephalitis. Coma often precedes death.
Gastro intestinal complications include hemorrhage and superficial mucosal erosion while renal involvement leads to varying degrees of renal failure. There may be jaundice along with DIC and multiple organ failure. Neurological features are common in seriously ill patients and range from restlessness, irritability, delirium, seizures to toxic encephalopathy leading to stupor and coma.
Wil Felix test (WF) using a proteus OXK strain gives positive test in 50% of patients during second week of illness. A minimum positive titer of 1: 80 or a four fold rise over previous levels is significant.
Other tests include Micro immuno fluorescence, latex agglutination, indirect haemagglutination, immuno peroxidase assay, ELISA and polymerase chain reaction (PCR). A dip stick test using a dot blot immunoassay format for the sero diagnosis of scrub typhus is accurate, rapid and easy to use test.
The leucocyte count is variable and there is neutropenia with relative lymphocytosis.
Tetra cycline 500 mg four times a day or doxycyclin 200 mg OD for seven days is the treatment of choice. For patients not responding to these drugs, Chloramphenicol 500 mg QID or Rifampacin 900 mg per day for a week are the alternative choices. Patient generally responds within 24-36 his after beginning of the treatment.
Besides drug, supportive measures are to be carried out. Relapse of the disease is unusual.
Prognosis. Earlier on scrub typhus carried a mortality of 8-50% but with the intraduction of newer therapeutic agents it has declined remarkably. Bad prognostic features include meningo encephalitis, ARDS, cardiac and peripheral circulatory failure.
Endemic Typhus (Murine typhus fever)
This is a milder form of it which occurs world wide. The acute fibrile illness is caused by Rickettsia mooseri (typhus) conveyed to man by rat flea (Xenopsylla cheopis) from infected rats or rodents.
The morphology of R. mooseri is similar to R. Prowazekii Invasion of the body by it provokes both specific and non-specific immunologic responses. Infection in humans occurs after the flea bite and contamination of broken skin by rickettsia laden faeces.
Clinical features of Typhus disease
The incubation period is generally from 8 tol4 days. The onset is rapid with high body temperature, chills, headache and arthralgia followed by nausea and vomiting. The face becomes flushed, conjunctiva suffused and features of pulmonary congestion appear.
The rash appear by the fourth or fifth day in axilla, chest, abdomen and inner surface of arms spreading to trunk, extremities, palms, soles and face. To start with the rash is in the form of rose red macules turning to maculo papular dusky red in color which fades on pressure. Petechiae are uncommon.
Fever lasts for 7 to 14 days. Complications include pulmonary congestion, broncho pneumonia Tachycardia, Hypo-tension, agitation, delirium and photo-phobia. Abdominal pain along with diarrhea is another feature. Renal functions generally remain unaffected.
The disease usually runs a mild course and recovery is smooth.
Diagnosis of brill zinsser
A positive 4bit Felix reaction to 0X19 strain of Proteus with negative agglutination to OXK and OX2 antigens will establish the diagnosis. A history of association with rodents is helpful.
Treatment and prevention of Typhus disease
Chloramphenicol and tetracyclines are the drugs of choice. After an initial loading dose, the drug has to be continued for 2 days after the temperature has been normal. For prevention of murine typhus, measures be adopted to eradicate rats and rat fleas by spraying of insecticides.