RICKETTSIAL INFECTIONS Flashcards
(19 cards)
What are RICKETTSIAL INFECTIONS: what diseases do they cause?
Rickettsiae are named after Howard T Ricketts, who identified them as causative agents of typhus and Rocky Mountain spotted fever.
The family rickettsiaceae consists of microorganisms that cause diseases which fall mainly in four major groups namely
1. typhus fevers,
2. spotted fevers,
3. Q-fever
4. trench fever.
Because of their obligate intracellular parasitism, they were thought to be close to viruses, but they are true bacteria
What is the Microbiology of rickettsial
- Highly fastidious
- Obligate intracellular parasites except Rochalimaea quintana
- Pleomorphic, usually seen as rods and in pairs
- Most species are gram-negative except C.burneti which is gram-positive
- Possess multilayered limiting membrane
- Limiting membrane digested by lysozyme
- Cell wall contains muramic acid
- Some organisms are capsulated
- Possess both RNA and DNA
- Multiply by binary fission
- Cannot pass through filters which hold conventional bacteria
- Susceptible to antibiotic therapy
- Primarily parasitic in arthropods
They are thus true bacteria, specially adapted to obligate intracellular parasitism. Rickettsiae appear as pleomorphic coccobacillary forms. They vary in length
from 0.25 to 2 μm.
These are sometimes observed in pairs or chains or filaments. C.burneti is the smallest, while the spotted fever rickettsiae are the largest. The
organisms are found within the nuclei or cytoplasm.
They are non-motile and non capsulated, are by and large gram-negative though they do not take the stain well.
Cultivation of Rickettsiae: where can they be found, which cell lines?
They are readily cultivated in the yolk sac of developing chick embryo. They also grow on continuous cell lines such as Hela, Hep2, Detroit 6; etc. but the growth is not satisfactory.
Laboratory animals such as guinea pigs and mice are useful for the isolation of rickettsiae from patients.
Rickettsiae do not grow in cell free media with the exception of Rochalimaea quintana which can grow on blood agar.
Discuss the Susceptibility of Rickettsiae to Physical and Chemical Agents
The organism of which disease is most resistant to dring?
Rickettsiae are readily inactivated by physical and chemical agents.
In general, rickettsiae are quickly destroyed by heat, drying and bactericidal chemicals.
Although rickettsiae are usually killed by storage at room temperature, dried faeces of infected lice may remain infective for months at room temperature.
The organism of Q-fever is most resistant to drying.
Antigenic Structure of Rickettsiae: what are the types of antigens?
Three types of antigens have been demonstrated.
- Group specific soluble antigen is present on the surface of the rickettsiae.
- Species specific antigen is associated with the body of the organism . In the case of scrub typhus it is strain specific.
- Polysaccharide antigen is the third antigen.It is an alkali stable polysaccharide found in some rickettsiae and in some strains of Proteus bacilli.
This sharing of antigens between rickettsiae and Proteus is the basis for the Weil-Felix reaction, which is used for diagnosis of rickettsial infections by demonstration of agglutinins of Proteus strains OX19, OX2 and OXK.
Pathogenesis of Rickettsiae
- Rickettsial diseases develop after infection through skin or respiratory tract.
- Ticks and mites transmit the agents of spotted fever and scrub typhus by inoculating the
rickettsia directly into the dermis during feeding. - The louse and flea, which transmit epidemic and murine typhus respectively, deposit infected faeces on the skin and the infection occurs when organisms are rubbed into the puncture wound made by the arthropod.
- The rickettsiae of Q-fever gain entry through the respiratory tract when infected dust is inhaled.
- Although organisms probably multiply at the original site of entry in all instances, local lesions appear with regularity only in certain diseases such as scrub typhus, etc.
- After multiplication at the local site these enter the blood stream.
- Rickettsiae multiply in endothelial cells of small blood vessels and produce vasculitis.
- The cells become swollen and necrotic, there is thrombosis of the vessel
leading to rupture and necrosis. - Vascular lesions are prominent in the skin but vasculitis occurs in many organs such as muscles, heart, lung and brain.
- In the brain, aggregations of lymphocytes, polymorphonuclear leucocytes and macrophages are associated with the blood vessels of the grey matter, these are called typhus nodules.
Clinical Features of the various Rickettsial infections
What is the characteristic feature of scrub typhus?
Except for Q-fever in which there is no skin lesion, rickettsial infections are characterized by:
fever, headache, malaise, prostration, skin rash and enlargement of spleen and liver.’
Q-fever resembles influenza and primary atypical pneumonia.
In epidemic typhus the rash is maculo-papular and appears on the fourth or fifth day of illness.
Endemic typhus presents same clinical picture but in a mild way.
An important feature of scrub typhus is the presence of punched out ulcer (eschar) covered with a blackened scab which indicates the site of bite.
The spotted fever group resembles typhus fever clinically.
Epidemic typhus
Causative organism? Also known as?
Louse-borne typhus is the prototype of the typhus group of rickettsial diseases.
The primary illness and its recrudescent form (Brill-Zinsser’s disease) is caused by Rickettsia prowazeki.
Louse-borne typhus is also known as epidemic typhus, classic typhus, typhus exanthematicus, and jail fever.
Pathogenesis and Pathology of epidemic typhus
- Following proliferation locally at the site of the louse bite, the organism presumably spreads haematogenously.
- R.prowazeki, like most rickettsiae, produces a vasculitis by infecting the endothelial cells of capillaries, small arteries, and veins.
- The process results in fibrin and platelet deposition, followed by occlusion of the vessel.
- Perivascular infiltration with lymphocytes, plasma cells, histiocytes, and polymorphonuclear leukocytes occurs with or without frank necrosis of the vessel.
Clinical Features of epidemic typhus
Following an incubation period of approximately one week, an abrupt onset with intense headache, chills, fever, and myalgia is characteristic. There is no eschar.
The fever worsens quickly (102-104°F), becomes unremitting, and the patient is soon prostrated by the illness.
A rash begins in the axillary folds and upper trunk on about the fifth day of illness. Within several days, the rash becomes maculopapular, darker, petechial, fixed and confluent and involves the entire body, sparing the face, palms, and soles.
Treatment and prevention of epidemic typhus
The antibiotics-chloramphenicol and tetracycline, are both effective against louse-borne typhus.
Prevention
Control of the human body louse and the conditions that foster its proliferation are the mainstay of prevention of louse-borne typhus.
BRILL-ZINSSER DISEASE
Cause? What is it precipitated by?
What does it resemble?
Brill-Zinsser disease occurs as a recrudescence of a previous infection with R. prowazeki. Its pathogenesis is unknown, but recurrence is presumed to be precipitated
by stress or a waning immune system. The illness is similar to louse-borne typhus but is usually milder and more closely resembles murine typhus.
Clinical Features of BRILL-ZINSSER DISEASE
After an incubation period of 1 to 2 weeks, the illness is characterized by headache, myalgia and fever. Onset is variable being gradual less often sudden. There is no
eschar.
Frequently a nonproductive cough occurs early in the course. Rash occurs in 60-80 per cent of the patients and first becomes evident on the third to fifth
day of illness.
The rash of murine typhus becomes maculopapular, and remains for 4-8 days. The rash may vary greatly in duration and intensity.
Treatment BRILL-ZINSSER DISEASE
Therapy with tetracycline or chloramphenicol produces defervescence in 2 days
Scrub Typhus
clinical features? causative organism?
Scrub typhus is a mite-borne illness characterized by fever, headache, rash, and an eschar at the site of the inoculating chigger bite.
It is endemic in southern and
eastern Asia, northern Australia, and the Western Pacific Islands.
Aetiologic Agent
Scrub typhus is caused by Rickettsia tsutsugamushiwhich is an obligate, intracellular bacterium seen best with the Giemsa stain in infected tissues.
Pathogenesis and pathology of scrub typhus
The infected chigger, while feeding, deposits rickettsiae into the tissue of the human host.
Multiplication takes place locally resulting in a cutaneous multiloculated vesicle which eventually ulcerates and forms a characteristic eschar with a black crust.
A rickettsemia has been demonstrated late in the incubation period.
Endothelial cells are infected during the haematogenous spread of the organism, and perivascular inflammation with mononuclear cells develops.
Lymphadenopathy and splenomegaly are common. Severe illness has been associated with pneumonia and myocarditis.
Clinical Manifestation & complication of scrub typhus
Six to 20 days after the infecting chigger bite, the patient suddenly becomes ill with fever, chill, headache, and myalgia.
Although usually on the extremities, the eschar may be found in other areas, particularly where skin surfaces come together, e.g. the axilla and scrotum.
If untreated, the fever will persist for 2 weeks or more and, among survivors, may fall gradually over several days.
Complications leading to death include pneumonia and circulatory collapse. Convalescence may be prolonged.
Treatment of scrub typhus
Scrub typhus is even more responsive to tetracycline and chloramphenicol than the other rickettsiosis, patients becoming afebrile within 24-36 hours of starting
therapy.
