Contents
Zoonotic diseases with worldwide distribution in foci of endemicity, with sporadic and often seasonal outbreaks.
Epidemiology
Rickettsial organisms have been found on all continents except Antarctica. Most rickettsial species are region-locked due to climatic conditions and vector and natural host constraints.

Vector lifecycle:
Rickettsiae require a vector for host transmission; however, infection is acquired by different routes depending on the vector type and rickettsial species. Most SFG rickettsiae are harbored by ixodid ticks and are transmitted by their bites during feeding (saliva). This is also true for most other rickettsiae that are harbored by mites. Flea- and louse-borne rickettsiae are known to cause infection via entry of fecal material in bite sites and cuts on the host’s skin. TG rickettsiae can cause infection via inhalation through the aerosolization or contamination of dust particles floating in the air. An uncommon route of infection is via the conjunctivae, through exposure of contaminated tick hemolymph on fingers from crushed ticks.

Microbiology
Rickettsiae:
Strictly intracellular bacteria that are vectored by various arthropods. To date, 18 species are recognized human pathogens, 12 of which cause CNS R
- Weakly gram positive
- Obligate intracellular
- Non-motile

Classification:
Classification into the two groups was historically based on their physiological characteristics of intracellular localization, optimal growth temperature, and cross-reaction of serum from an infected patient with somatic antigens of three strains of Proteus. The classification of new members of Rickettsia today is done through genomic sequence comparison with information for well-published strains.

Spotted fever group (SFG) rickettsioses:
- Rocky Mountain spotted fever (RMSF)| R. rickettsii
- Mediterranean spotted fever (MSF) | R. conorii
- Japanese spotted fever (JSF) | R. japonica
- Tick-borne lymphadenopathy (TIBOLA)/Dermacentor-borne necrosis erythema and lymphadenopathy (DEBONEL)/Scalp eschar and neck lymphadenopathy after tick bite (SENLAT) | R. slovaca and R. raoultii
- African tick bite fever (ATBF) | R. africae
- R. helvetica infection
Typhus group (TG) rickettsiae:
- Epidemic typhus | R. prowazekii
- Murine/endemic typhus | R. typhi
Transitional group rickettsiae:
- Rickettsial pox | R. akari transmitted by the mite, Liponyssoides sanguineus
- Queensland tick typhus (QTT) | R. australis transmitted by Ixodes ticks
- Flea-borne spotted fever | R. felis transmitted by fleas, Ctenocephalides felis
Scrub typhus
- Orientia (O. tsutsugamushi and O. chuto)
Pathophysiology
Rickettsia and Orientia species are transmitted by the bite of infected ticks or mites or by the feces of infected lice or fleas. From the portal of entry in the skin, rickettsiae spread via the bloodstream to infect the endothelium and sometimes the vascular smooth muscle cells. Rickettsia species enter their target cells, multiply by binary fission in the cytosol, and damage heavily parasitized cells directly.
Lymphohistiocytic vasculitis:
Damage to small blood vessels lead to extravasastion of fluid leading into interstitial space
- Oedema, hypovolemia, hypotension, hypoalbuminemia
- Complications: Encephalitis (CNS), myocarditis (heart), pulmonary oedema
Procoagulant state:
Due to activation of platelets & fibrinolytic system
- Thrombi
Rickettsial neuroinvasion:
Occurs during the systemic phase of the disease and typically follows bacterial dissemination via the bloodstream via a transcellular approach

Presentation
Rickettsia species cause Rocky Mountain spotted fever, rickettsial pox, other spotted fevers, epidemic typhus, and murine typhus. Orientia (formerly Rickettsia) tsutsugamushi causes scrub typhus. Patients present with febrile exanthems and visceral involvement; symptoms may include nausea, vomiting, abdominal pain, encephalitis, hypotension, acute renal failure, and respiratory distress.
Clinical manifestations of rickettsial disease range from a mild, self-limiting illness to life-threatening multi-organ failure.
Spotted fever group (SFG) rickettsioses:
- Clinical triad: Fever, inoculation eschar(s), and generalized cutaneous rash
- Other faetures: Nonspecific flu-like symptoms, isolated fever, myalgia, cough, generalized lymphadenopathy, abdominal pain

TG ricket:
- Red maculopapulat rash (HALLMARK feature, which starts at trunk and spreades to extremities sparing hands, feet and head)
- Complication: Brill-Zinsser disease
Diagnosis
The diagnosis of a rickettsial infection is usually achieved through the gathering of a complete clinical history indicating exposure to a potential source of rickettsial disease alongside laboratory testing. The submission of arthropods collected at the bite site or eschar for rickettsial detection is also recommended if available.

Laboratory findings:
- Thrombocytopenia
- ↑ PT & aPTT
- Transaminitis
- Hyponatremia
Tissue biopsy:
Indirect immunofluorescence (IFA)

Management
It is important to recognise rickettsial infections early in their disease course as they can lead to life-threatening multi-organ failure if specific anti-rickettsial antimicrobial therapy is not prescribed promptly.
Antibiotic therapy:
M/efficient antibiotics to cure rickettsioses are tetracycline derivatives, primarily doxycycline
- Doxycycline 200 mg (for 7 days or until 2 days after apyrexia is obtained)
- Severe forms: IV doxycycline
- Alternative: Chloramphenicol and macrolides (azithromycin, clarithromycin, and roxytromycin)