Rickettsiosis (overview) A75-79

The pathogens were named after the pathologist Howard Taylor Ricketts (1871-1910), who, among other things, researched Rocky Mountain spotted fever, the pathogens of which he was able to detect in the blood of infected people (vector = tick species). In 1909 he traveled to Mexico City with the aim of researching typhus. In the process, he became infected with rickettsiae and died in 1910.

Infectious diseases caused by rickettsiae (bacteria-like pleomorphic cocci), transmitted via various arthropods (e.g. ticks, lice, fleas) and occurring worldwide, see Table 1.

Some rickettsial infections are transmitted by ticks, mites or mite larvae, others by lice or fleas (see table).

In the case of tick-borne infections (tick-borne), the pathogen is transmitted to humans via the salivary glands with the bite.

In the case of rickettsial infections caused by lice or fleas, the pathogens are found in the faeces of the animals and enter skin lesions, for example by scratching.

In the case of infections transmitted by ticks or mites, a primary lesion (eschar) and lymphadenitis occur after inoculation of the pathogen.

The incubation period is 1 to 2 weeks. In case of exposure, the occurrence of fever, eschar and exanthema should be considered as a differential diagnosis of rickettsialpox. Rickettsiosis is clinically manifested by high fever, myalgia, arthralgia, maculo-papular exanthema and swelling of the lymph nodes. Typical complications are thrombosis and thrombophilia, which are manifested by petechiae as well as gastrointestinal bleeding. Other complications include encephalitis, myocarditis, nephritis, hemorrhages, and gangrene.

Note: Rickettsiosis must also be excluded in cases of fever of unknown origin (FUO).

Further diagnostics are recommended if the clinical picture is typical. The pathogen can be detected indirectly or directly.

Direct pathogen detection:

• immunofluorescence microscopy (antigen detection) from tissue samples (spleen, lungs, skin)
• Nucleic acid detection by PCR from affected material

Indirect detection:

• specific antibodies (IgM, IgG by ELISA, IFT, CFT)

Earlier detection by Weil-Felix reaction. Today, more specific serological tests such as molecular biological techniques are available to identify the pathogens from blood and tissue. Detection of IgM and IgG antibodies using ELISA, immunoperoxidase techniques.

Remember! Start therapy already with clinical suspicion of rickettsialpox (serology takes 2 weeks)!

Drug of choice is tetracycline p.o. (e.g. Tetracycline Wolff 500) 250 mg every 6 hrs. (or 25-50 mg/kg bw/day) for 8-12 days, approx. 5 days beyond the absence of fever and symptoms. Doxycycline (e.g. Doxy-Wolff) 100 mg p.o. 2 times/day for 8-10 days is also effective. Alternatively: Ciprofloxacin 2 times/day 500-750 mg p.o. or 2 times/day 100-200 mg i.v.

In the most severe cases with incipient haematogenous spread or generalisation, also glucocorticoids i.v. to counteract the toxic immune reaction triggered by the decay of the bacteria. Prednisolone (e.g. Decortin H) 100-125 mg/day for 2-3 days.

Notice. Especially in classical spotted fever and Rocky Mountains spotted fever, life-threatening situations can occur that make intensive medical care necessary.

The following measures are recommended
:- delousing of persons and clothing

- close contact persons of patients possibly doxycycline prophylaxis (single dose)

- a vaccine is available for particularly endangered groups of persons, e.g. medical personnel in endemic areas or persons in special laboratories.

Classification of rickettsial diseases:

Infection by Reckiettsia conori:

3 days after a holiday stay in South Africa a 46 years old patient fell ill with flu-like symptoms with fatigue, medium fever and catarrhal symptoms. At the same time a rather discreet, not itchy, bright red, truncated, maculo-papular (0.1-0.2 cm large efflorescences) exanthema developed.

Findings: A 0.5 cm large ulcer with blackish crusts (tache noir) was found on the extensor lower leg. A slightly painful regional lymphadenopathy was striking. The blood count showed clear leukopenia (2,200/ul) and monocytosis (15.5%). On admission no positive rickettsial serology. Only 5 weeks later clearer IgG-titer (1:320) on R. conori.

Therapy: Doxycycline 2 times/day 100 mg p.o. for 10 days. Immediate clinical improvement. Ulcer healed under usual wound treatment after 6 weeks.

1. Baumann D et al (2003) Fever after a tick bite: clinical manifestations and diagnosis of acute tick bite-associated infections in northeastern Switzerland. Dtsch Med Weekly 128: 1042-1047
2. Diaz IA et al (2003) Rickettsiosis caused by Rickettsia conorii in Uruguay. Ann N Y Acad Sci 990: 264-266
3. Lee HC et al (2002) Clinical manifestations and complications of rickettsiosis in southern Taiwan. J Formos Med Assoc 101: 385-392
4. Murray KO et al (2017) Typhoid Group Rickettsiosis, Texas, USA, 2003-2013 Emerg Infect Dis 23:645-648 .
5. Orfanos CE et Garbe C: Rare infections of the skin. In: Therapy of skin diseases. Orfanos CE (Ed.). Springer-Verlag Berlin Heidelberg New York. S. 173–176
6. Oteo JA et al (2003) Epidemiological and clinical differences among Rickettsia slovaca rickettsiosis and other tick-borne diseases in Spain. Ann N Y Acad Sci 990: 355-356
7. Raoult D et al (2002) Spotless rickettsiosis caused by Rickettsia slovaca and associated with Dermacentor ticks. Clin Infect Dis 34: 1331-1336
8. Toutous-Trellu L et al (2003) African tick bite fever: not a spotless rickettsiosis! J Am Acad Dermatol 48: S18-19