Rickettsia
Definition ★★★
Prokaryotes that are obligate intracellular parasites. They are transmitted to humans by arthropod vectors.
The deck's key-points slide adds the essentials: Rickettsia are pleomorphic coccobacilli, obligate intracellular pathogens similar to Gram-negative bacteria, but they DO NOT stain with the Gram stain. The hallmark of infection with Rickettsia is VASCULITIS. Doxycycline is the drug of choice.
| Family | Genera |
|---|---|
| Rickettsiaceae | Rickettsia · Orientia |
| Anaplasmataceae | Anaplasma · Ehrlichia · Neorickettsia · Wolbachia |
Five of the six genera are pathogenic to humans.
- Define Rickettsia. → Prokaryotes that are obligate intracellular parasites, transmitted to humans by arthropod vectors
- What is the hallmark of rickettsial infection? → Vasculitis
- Do they Gram stain? → No — although their wall resembles that of Gram-negative bacteria
⭐ Common properties ★★★
“Please list the common properties of rickettsia” is question 6 on the TMU homework list — brief-answer shape. Here is the deck's list in full.
- Small (Ø 0.3–1.0 µm), pleomorphic, coccobacillary
- Resemble Gram-negative bacteria in their cell wall; no flagella, no spores
- Obligate intracellular parasites
- Contain BOTH DNA and RNA
- Reproduce by binary fission
- Arthropods are their vectors and/or reservoirs — ticks, mites, lice or fleas
- Cause zoonoses
- Sensitive to antibiotics
- Exclusively infect the endothelial cells of small blood vessels
- Produce fever, headache and a petechial rash
| Detail | |
|---|---|
| Cultivation | In living tissues only — embryonated chicken eggs and vertebrate cells. Cultivation is costly and hazardous, because aerosol transmission easily occurs |
| Sensitive to | Heat — inactivated at 56 °C in 30 min · antibiotics |
| Resistant to | Dryness — survives more than 1 year in dry tick faeces |
This module contains four organisms that are all “not quite bacteria”, and the examiner is testing whether you can tell them apart. Three of the properties above do the work.
Contains both DNA and RNA, and divides by binary fission. That is a bacterium, not a virus — a point the deck makes deliberately, because obligate intracellular growth is otherwise a viral trait. A virus has one nucleic acid and does not divide.
Sensitive to antibiotics. Same argument, and it is the clinically decisive one.
Obligate intracellular parasite. This is what separates Rickettsia and Chlamydia from Mycoplasma, which grows freely on artificial medium.
So: Mycoplasma = smallest, no wall, grows free. Rickettsia and Chlamydia = have a wall, but cannot grow outside a cell. And Rickettsia is the one with an arthropod vector — which is how Unit 16 will distinguish the two.
- List the common properties of Rickettsia. → Small (0.3–1.0 µm) pleomorphic coccobacilli · G−-like wall, no flagella or spores · obligate intracellular · both DNA and RNA · binary fission · arthropod vectors/reservoirs (ticks, mites, lice, fleas) · zoonoses · antibiotic-sensitive · infect endothelial cells of small vessels · fever, headache, petechial rash
- How are they cultivated? → Only in living tissue — embryonated chicken eggs and vertebrate cells; costly and hazardous because of aerosol transmission
- What are they sensitive and resistant to? → Sensitive to heat (56 °C/30 min) and antibiotics; resistant to dryness — over a year in dry tick faeces
- How do you know Rickettsia is a bacterium and not a virus? → It contains both DNA and RNA, divides by binary fission, and is antibiotic-sensitive
Pathogenesis ★★★
| Route of infection | Detail |
|---|---|
| Sting or bite / skin abrasion | The usual route — often by scratching infected arthropod faeces into the bite |
| Respiratory tract | Inhaling aerosols containing rickettsiae |
| Eye mucous membrane |
| Virulence factor | Action |
|---|---|
| LPS | Endotoxin |
| Phospholipase A | Destroys the phagosome |
| Direct injury | To the endothelial cells of small blood vessels |
The pathogenic sequence
Arthropod (vector, reservoir) → sting/bite, scratching or inhalation → rickettsiae invade → preferentially infect the endothelial cells of small blood vessels → disseminate in the bloodstream to many organs (skin, brain, heart) → destruction of small blood vessels → blood leakage → decrease in blood volume → endotoxaemia and shock. Clinically: fever, headache and a petechial rash.
Exclusively infect the endothelial cells of small blood vessels. Hold that single fact and the entire clinical picture follows without memorising it.
Endothelium is the lining of every small vessel in the body. Destroy it and vessels leak.
• Leak in the skin → the petechial rash, which is haemorrhage, not inflammation — and which is why the deck notes that in epidemic typhus the macular rash becomes haemorrhagic.
• Leak in the brain → headache, then CNS dysfunction.
• Leak in the heart → myocarditis.
• Leak everywhere at once → loss of intravascular volume → shock, which is what kills.
This is why the deck calls vasculitis the hallmark. It is not one of several features; it is the disease.
- Name the three routes of infection. → Sting or bite / skin abrasion · inhalation of aerosols · eye mucous membrane
- Name the three virulence factors. → LPS endotoxin · phospholipase A (destroys the phagosome) · direct injury to vascular endothelium
- Give the pathogenic sequence. → Arthropod bite → invasion → endothelial cells of small vessels → bloodstream dissemination to skin, brain and heart → vessel destruction → blood leakage → reduced blood volume → endotoxaemia and shock
- Why is the rash petechial? → It is haemorrhage from destroyed small vessels, not inflammation
The three important rickettsioses ★★★
| Disease | Causative agent | Vector | Main reservoir |
|---|---|---|---|
| Epidemic typhus (louse-borne typhus) | R. prowazekii | Body louse | Human |
| Endemic typhus (murine typhus, flea-borne fever) | R. typhi | Rat flea | Wild rodents (rats) |
| Scrub typhus | O. tsutsugamushi | Mite | Wild rodents |
Epidemic typhus
| Detail | |
|---|---|
| Source | Patients — humans are the reservoir |
| Transmission | Person → person by the body louse, which bites and defecates in the wound |
| Incubation | 5–15 days |
| Occurrence | Crowded areas, especially with poor sanitation — causing epidemics |
| Symptoms | Fever, chills, headache, myalgia, arthralgia, macular rash (trunk → extremities), the macular rash becoming haemorrhagic |
| Complications | Myocarditis, CNS dysfunction |
| Mortality | High — 60–70% in untreated cases |
Endemic (murine) typhus
| Detail | |
|---|---|
| Reservoir | Rodents (rats) |
| Vector | Rat flea — rat → rat, and rat flea → human |
| Incubation | 8–12 days |
| Symptoms | Similar to epidemic typhus, but MILDER; no complications |
| Mortality | Less than 1% |
| Occurrence | Sporadic, in tropical and subtropical coastal regions and ports with large numbers of rats |
Scrub typhus
| Detail | |
|---|---|
| Hosts | Rats and other small mammals |
| Vector | The larval stage (chigger) of mites — Leptotrombidium |
| Symptoms | Fever, headache, spotted rash, ESCHAR, swelling of the lymph glands |
Two typhus fevers, similar organisms, and a seventyfold difference in death rate. The reason is in the reservoir column.
Epidemic typhus has a HUMAN reservoir and a human vector — the body louse, which lives in clothing. It therefore spreads person to person wherever people are crowded together and cannot wash or change clothes: refugee camps, prisons, armies in winter. That is why it is epidemic, and why it has killed in wars for centuries. Untreated mortality 60–70%.
Endemic typhus has a RAT reservoir and reaches humans only by accident, when a rat flea bites the wrong host. There is no human-to-human amplification, so cases are sporadic. Mortality under 1%.
Scrub typhus has its own marker: the eschar at the chigger bite — a black necrotic scab, the single most useful physical sign in the group, and the same word used for cutaneous anthrax in Unit 12.
- Name the three rickettsioses with agent, vector and reservoir. → Epidemic typhus — R. prowazekii, body louse, human · endemic (murine) typhus — R. typhi, rat flea, wild rodents · scrub typhus — O. tsutsugamushi, mite, wild rodents
- Describe epidemic typhus. → Person-to-person by the body louse which bites and defecates in the wound; incubation 5–15 days; crowded, insanitary conditions; fever, chills, headache, myalgia, arthralgia, macular rash from trunk to extremities becoming haemorrhagic; myocarditis and CNS dysfunction; 60–70% mortality untreated
- How does endemic typhus differ? → Rat reservoir and rat-flea vector, incubation 8–12 days, milder, no complications, mortality under 1%
- What is the distinguishing sign of scrub typhus? → An eschar at the mite (chigger) bite, with lymph node swelling
⭐ The Weil-Felix reaction ★★★
An agglutination test performed to detect rickettsial antibody that can agglutinate certain strains of Proteus vulgaris (OX-2, OX-19, OX-K), helping to diagnose rickettsial disease.
| Disease (agent) | Proteus strain agglutinated |
|---|---|
| Epidemic typhus (R. prowazekii) | OX-19 |
| Murine typhus (R. typhi) | OX-19 |
| Scrub typhus (O. tsutsugamushi) | OX-K |
| Rocky Mountain spotted fever (R. rickettsii) | OX-19, OX-2 |
Limitations: it is non-specific and insensitive. Proteus infection must be excluded, and the result must be referred to the clinical manifestations, history of exposure, and seasonal and geographic epidemiology.
The principle is the mark most students miss: it works because certain Rickettsia share a common polysaccharide antigen with those Proteus strains, so anti-rickettsial antibody cross-reacts with and agglutinates the far more easily cultured Proteus. The test detects antibody to Rickettsia using Proteus as the antigen.
The results: OX-19 for epidemic and murine typhus, OX-K for scrub typhus, OX-19 and OX-2 for Rocky Mountain spotted fever.
The limitation earns the last mark: it is non-specific and insensitive, Proteus infection must be excluded, and it must be interpreted with the clinical and epidemiological picture.
Direct detection is also possible: in tissues such as skin biopsy, by Giemsa stain — a bluish-purple colour — or, as a timely, rapid diagnostic procedure, by immunofluorescent test.
- Define the Weil-Felix reaction. → An agglutination test detecting rickettsial antibody that agglutinates certain strains of Proteus vulgaris (OX-2, OX-19, OX-K), used to diagnose rickettsial disease
- Why does it work? → Rickettsiae share a common polysaccharide antigen with those Proteus strains, so the antibody cross-reacts
- Which strain for scrub typhus? → OX-K
- Which for epidemic and murine typhus? → OX-19
- What are its limitations? → Non-specific and insensitive; Proteus infection must be excluded and results interpreted with the clinical and epidemiological picture
- How else can Rickettsia be detected directly? → Giemsa stain of tissue such as skin biopsy (bluish purple), or immunofluorescence
Treatment, prevention and control ★★
| Detail | |
|---|---|
| Treatment | Tetracycline, chloramphenicol (doxycycline is the drug of choice) |
| ⚠️ CONTRAINDICATED | The sulfonamides — they STIMULATE rickettsial growth |
| Control | Cleanliness, sanitation and personal hygiene · protective clothing · insect repellents and insecticides |
| Vaccine | Under study |
The sulfonamide point is the kind of single fact examiners like: an antibiotic that makes the disease worse. Note too that control is vector control — as with plague in Unit 12, breaking the arthropod link is the intervention that works.
- How is rickettsial disease treated? → Tetracycline or chloramphenicol; doxycycline is the drug of choice
- Which drugs are contraindicated, and why? → The sulfonamides — they stimulate rickettsial growth
- How is it controlled? → Cleanliness, sanitation and personal hygiene; protective clothing; insect repellents and insecticides. No vaccine yet
Revision
The deck's summary slide and its multiple-choice
It names the common properties · the pathogenesis and main rickettsioses · definitions: Rickettsia and the Weil-Felix reaction. Its question — “The vector of Rickettsia prowazekii is…” — has the answer A. human (body) louse.
The whole unit on one screen
| Question | Answer |
|---|---|
| Definition? | Prokaryotes that are obligate intracellular parasites, transmitted by arthropod vectors |
| Hallmark? | Vasculitis |
| Target cell? | Endothelial cells of small blood vessels |
| Nucleic acid? | Both DNA and RNA — it is a bacterium |
| Culture? | Living tissue only — embryonated eggs, vertebrate cells |
| Resistance? | Killed at 56 °C/30 min; survives >1 year in dry tick faeces |
| Virulence? | LPS endotoxin · phospholipase A · direct endothelial injury |
| Epidemic typhus? | R. prowazekii · body louse · human reservoir · 60–70% mortality |
| Endemic typhus? | R. typhi · rat flea · rodents · <1% |
| Scrub typhus? | O. tsutsugamushi · mite (chigger) · rodents · eschar |
| ⭐ Weil-Felix? | Agglutination of Proteus vulgaris OX-19 / OX-2 / OX-K by rickettsial antibody; OX-K = scrub typhus |
| Treatment? | Tetracycline, chloramphenicol, doxycycline. NEVER sulfonamides |
- Define the Weil-Felix reaction for 4 marks. → An agglutination test detecting rickettsial antibody that cross-reacts with and agglutinates Proteus vulgaris OX-2, OX-19 and OX-K, thanks to a shared polysaccharide antigen; OX-19 for epidemic and murine typhus, OX-K for scrub typhus; non-specific and insensitive
- List the common properties of Rickettsia. → Small pleomorphic coccobacilli with a G−-like wall · no flagella or spores · obligate intracellular · both DNA and RNA · binary fission · arthropod vectors · zoonoses · antibiotic-sensitive · infect small-vessel endothelium · fever, headache, petechial rash
- Why is the disease a vasculitis? → The organism exclusively infects small-vessel endothelium; its destruction causes leakage — rash, CNS and cardiac involvement, and shock
- Which vector for each typhus? → Body louse (epidemic) · rat flea (endemic) · mite (scrub)
- Which drug class must be avoided? → The sulfonamides — they stimulate rickettsial growth