TYPHUS FEVER.pptx

It is a type of Infectious disease caused by the Rickettsia genus of bacteria.
Rickettsiae are a heterogeneous group of small, obligately intracellular, gram-negative coccobacilli and short bacilli, most of which are transmitted by a tick, mite, flea, or louse vector.
Except in the case of louse-borne typhus, humans are incidental hosts.

1. TYPHUS FEVER Dr,Jyoti Verma Associate Professor Medicine department

2. What is Typhus fever? It is a type of Infectious disease caused by the Rickettsia genus of bacteria. Rickettsiae are a heterogeneous group of small, obligately intracellular, gram-negative coccobacilli and short bacilli, most of which are transmitted by a tick, mite, flea, or louse vector. Except in the case of louse-borne typhus, humans are incidental hosts.

3. Features of Selected Rickettsial Infections causing typhus fever.

4. Clinical infections with rickettsiae can be classified according to (1) the taxonomy and diverse microbial characteristics of the agents, which belong to seven genera (Rickettsia, Orientia , Ehrlichia , Anaplasma , Neorickettsia , “ Candidatus Neoehrlichia ,” and Coxiella ); (2) epidemiology; or (3) clinical manifestations. The clinical manifestations of all the acute presentations are similar during the first 5 days: fever, headache, and myalgias with or without nausea, vomiting, and cough . As the course progresses, clinical manifestations—including a macular, maculopapular, or vesicular rash; eschar; pneumonitis; and meningoencephalitis —vary from one disease to another.

5. Heightened clinical suspicion is based on epidemiologic data history of exposure to vectors or reservoir animals travel to endemic locations clinical manifestations (sometimes including rash or eschar), and characteristic laboratory findings (including thrombocytopenia, normal or low white blood cell [WBC] counts, elevated hepatic enzyme levels, and hyponatremia ). Such suspicion should prompt empirical treatment.

6. EPIDEMIC (LOUSE-BORNE) TYPHUS The human body louse ( Pediculus humanus corporis ) lives in clothing under poor hygienic conditions and usually in impoverished cold areas Lice acquire R. prowazekii when they ingest blood from a rickettsemic patient The rickettsiae multiply in the louse’s midgut epithelial cells and are shed in its feces. The infected louse leaves a febrile person and deposits infected feces on its subsequent host during its blood meal The patient autoinoculates the organisms by scratching . The louse is killed by the rickettsiae and does not pass R. prowazekii to its offspring.

7. EPIDEMIOLOGY Epidemic typhus haunts regions afflicted by wars and disasters. An outbreak involved 100,000 people in refugee camps in Burundi in 1997 . A small focus was documented in Russia in 1998 , sporadic cases were reported from Algeria , and frequent outbreaks occurred in Peru and Rwanda . Eastern flying squirrels ( Glaucomys volans ) and their lice and fleas maintain R. prowazekii in a zoonotic cycle. Brill-Zinsser disease is a recrudescent illness occurring years after acute epidemic typhus, probably as a result of waning immunity. R. prowazekii remains latent for years; its reactivation results in sporadic cases of disease in louse-free populations or in epidemics in louse infested populations. Recrudescence has been documented after flying squirrel–associated typhus. Rickettsiae are potential agents of bioterrorism.

8. Clinical Manifestations After an incubation period of ~1–2 weeks , Severe headache, and fever rising rapidly to 38.8°–40.0°C (102°–104°F). Cough is prominent, developing in 70% of patients. Myalgias are usually severe. A rash begins on the upper trunk, usually on the fifth day, and then becomes generalized, involving the entire body except the face, palms, and soles. Initially, this rash is macular; becomes maculopapular, petechial, and confluent.

9. Clinical features cont. Photophobia , with considerable conjunctival injection and eye pain, is common. The tongue may be dry, brown, and furred. Confusion and coma are common. Skin necrosis and gangrene of the digits Interstitial pneumonia may occur in severe cases. Patients with untreated infections develop renal insufficiency and multiorgan involvement . Neurologic involvement(12%). Infection associated with North American flying squirrels is a milder illness; whether this milder disease is due to host factors (e.g., better health status) or attenuated virulence is unknown.

10. Diagnosis and Treatment Epidemics can be recognized by the serologic or immunohistochemical diagnosis of a single case or by detection of R. prowazekii in a louse found on a patient. Doxycycline (100 mg bid) is administered orally or—if the patient is comatose or vomiting— intravenously and continued until 3–5 days after defervescence . Under epidemic conditions, a single 200-mg oral dose can be tried but fails in some cases. Pregnant patients should be evaluated individually and treated with chloramphenicol early in pregnancy or, if necessary, with doxycycline late in pregnancy.

11. ENDEMIC MURINE TYPHUS R. typhi is maintained in mammalian host–flea cycles, with rats ( Rattus rattus and R. norvegicus ) and the Oriental rat flea ( Xenopsylla cheopis ) as the classic zoonotic niche. Fleas acquire R. typhi from rickettsemic rats and carry the organism throughout their life span. Nonimmune rats and humans are infected when rickettsia-laden flea feces contaminate pruritic bite lesions; less frequently, the flea bite transmits the organisms. Transmission can also occur via inhalation of aerosolized rickettsiae from flea feces. Infected rats appear healthy, although they are rickettsemic for ~2 weeks.

12. Epidemiology Murine typhus occurs mainly in Texas and southern California, where the classic rat–flea cycle is absent and an opossum–cat flea (C. felis ) cycle is prominent. Globally, endemic typhus occurs mainly in warm (often coastal) areas throughout the tropics and subtropics , where it is highly prevalent though often unrecognized. The incidence peaks from April through July in southern Texas and during the warm months of summer and early fall in other geographic locations.

13. Clinical Manifestations The incubation period of experimental murine typhus averages 11 days (range, 8–16 days). Headache, myalgia, arthralgia , nausea, and malaise develop 1–3 days before onset of chills and fever. Nausea and Vomiting . The duration of untreated illness averages 12 days (range, 9–18 days). Rash is present in only 13% of patients at presentation for medical care (usually ~4 days after onset of fever), appearing an average of 2 days later in half of the remaining patients and never appearing in the others.(axilla or the inner surface of the arm) Subsequently, the rash becomes maculopapular, involving the trunk more often than the extremities; it is seldom petechial and rarely involves the face, palms, or soles. A rash is detected in only 20% of patients with darkly pigmented skin.

14. Clinical manifestations cont. Pulmonary involvement is frequently prominent; 35% of patients have a hacking, nonproductive cough, and chest radiography have pulmonary densities due to interstitial pneumonia, pulmonary edema, and pleural effusions . Bibasilar rales are the most common pulmonary sign. Less common clinical manifestations include abdominal pain, confusion, stupor, seizures, ataxia, coma, and jaundice. Clinical laboratory studies Anemia and leukopenia early in the course, leukocytosis late in the course , Thrombocytopenia, hyponatremia, hypoalbuminemia, increased serum levels of hepatic aminotransferases, and prerenal azotemia . Complications can include respiratory failure, hematemesis, cerebral hemorrhage, and hemolysis

15. Diagnosis and Treatment Serologic studies of acute- and convalescent-phase serum samples can provide a diagnosis, and an immunohistochemical method for identification of typhus group specific antigens in biopsy samples has been developed. When endemic typhus is suspected, patients should be treated empirically with doxycycline (100 mg twice daily by mouth for 7–15 days). Chloramphenicol and ciprofloxacin are less effective alternatives.

16. SCRUB TYPHUS Epidemiology and pathophysiology O. tsutsugamushi is maintained by transovarial transmission in trombiculid mites . After hatching, infected larval mites (chiggers, the only stage that feeds on a host) inoculate organisms into the skin. Infected chiggers are particularly likely to be found in areas of heavy scrub vegetation during the wet season, when mites lay eggs. Scrub typhus is endemic and reemerging in eastern and southern Asia, northern Australia, and islands of the western Pacific and Indian Oceans.

17. Clinical Manifestations Illness varies from mild and self limiting to fatal. After an incubation period of 6–21 days, onset is characterized Fever, headache, myalgia, cough, and gastrointestinal symptoms. The classic case description includes an eschar where the chigger has fed, regional lymphadenopathy, and a maculopapular rash—signs that are seldom seen in indigenous patients. In fact, fewer than 50% of Westerners develop an eschar, and fewer than 40% develop a rash (on day 4–6 of illness). Encephalitis and interstitial pneumonia due to vascular injury. The case–fatality rate for untreated classic cases is 7% but would probably be lower if all mild cases were diagnosed.

18. Diagnosis and Treatment Serologic assays (indirect fluorescent antibody, indirect immunoperoxidase , and enzyme immunoassays ) are the mainstays of laboratory diagnosis. PCR amplification of Orientia genes from eschars and blood also is effective. Patients are treated with oral doxycycline (100 mg twice daily for 7–15 days), azithromycin (500 mg for 3 days), or chloramphenicol (500 mg four times daily for 7–15 days).

19. THAT’s ALL….