clinical

• Rickettsia


  • Gram-negative, but stain poorly
  • Small, rod-like or coccobacillary in shape
  • Grow only inside living host cells
  • Transmitted by infected tick
  • Not routinely cultured because of obligate intracellularity
• Pathogenesis of Rickettsia


  1. Transmitted to humans by arthropods, such as fleas, ticks, mites, and lice

  2. Rodents, humans, or arthropods can serve as reservoirs of infectious organisms

  3. Degrade the phagosome membrane by production of a phospholipase
• Mode of infection


  Rickettsia enter into the blood which are attach the endothelial cells and cause vasculitis (rash, oedema, haemorrhage)
• Vasculitis


  Inflammation of endothelial of blood vessels
• Spotted fever group


  • R. rickettsii (tick)
  • R. cnorii (tick)
  • R. akari (Mite)
• Rocky Mountain spotted fever


  A potentially lethal, but usually curable tickborne disease, and is the most common rickettsial infection in the United States
• Transmission of Rocky Mountain spotted fever


  1. Bite of an infected wood or dog tick

  2. Transovarian transmission
• Rocky Mountain spotted fever


  • High fever, malaise, and a prominent rash that begins on the palms and soles, and then spreads to cover the body
  • Rash can progress from macular to petechial or frankly haemorrhagic
  • Untreated, infection can lead to myocardial or renal failure
  • Mortality rates are highest (5 to 30 percent) among individuals older than 40 years of age
• Typhus group


  • Louse-borne (epidemic) typhus
  • Murine (endemic) typhus
  • Scrub typhus
• Transmission of louse-borne (epidemic) typhus

  1. R.prowazekii is transmitted from person to person by an infected human body louse that excretes organisms in its feces

  2. Scratching louse bites facilitates the introduction of the pathogen from louse feces into a bite wound

  3. Infected lice are themselves eventually killed by the infecting bacterium
• Louse-borne (epidemic) typhus


  • Occurs most typically in large epidemics under conditions of displacement of people, crowding, and poor sanitation
  • Pathogen is probably transmitted from flying squirrels to humans via body louse that excretes organisms in its faeces into a bite wound (rubbing faeces into broken skin), not by biting or zoonotic
• Symptoms of louse-borne (epidemic) typhus

  1. High fever, chills, severe headache which are entry into blood during one week and cause vasculitis that damage of brain or heart blood vessels

  2. Rash spreads centrifugally from trunk to extremities

  3. Disease lasts 2 weeks or longer, and tends to be more severe in older individuals

  4. Complications may include central nervous system dysfunction, myocarditis, and death
• Brill-Zinsser disease


  A usually milder form of typhus that occurs in persons who previously recovered from primary infections (10 to 40 years earlier)
• Latent infection


  Thought to be maintained in the reticuloendothelial system and probably serves as a reservoir for the organism in interepidemic periods
• Murine (endemic) typhus


  A clinically similar but usually milder disease than that caused by R. prowazekii
• Transmission of murine (endemic) typhus


  Human infections are initiated by the bites of infected rat fleas, and a worldwide reservoir for R. typhi exists in urban rodents
• Scrub typhus


  Transmission through Orienta tsutsugamushi by Rodent-mite-cycle
• Laboratory identification


  1. Specimens are blood or skin biopsy

  2. Serologic procedures rely on the demonstration of a rickettsia-specific antibody response during the course of infection

  3. Indirect fluorescent antibody tests using rickettsia-specific antibodies are available, primarily in reference laboratories

  4. Infected cells can be detected by immunofluorescence or histochemical procedures on some clinical samples such as punch biopsies from areas of rash

  5. Polymerase chain reaction (PCR) amplification can also be employed for the specific diagnosis of rickettsial diseases

  6. Isolation ex. Yolk sac of embryonated egg culture, tissue culture, guine pig or mice
• Treatment


  Tetracycline as first choice, Chloramphenicol as a secondary choice
• Prevention


  • Personal hygiene
  • No anti-rickettsial vaccine is licensed in the United States, and no preventive drug is available
  • Prevention depends on vector control, wearing proper clothing that minimizes bare skin, and immediate removal of attached ticks
• Vectors


  • Body louse
  • Fleas
  • Ticks
• Coxiella burnetii


  • Gram negative
  • Coccobacilli
  • Pleomorphic
  • Small size
  • Obligate intracellular
  • DNA and RNA
  • Binary fusion
  • Sensitive to antibiotics
• Coxiella burnetii, the causal agent of Q fever, is found worldwide (the "Q" stands for "query" because the cause of the fever was unknown for many years)
• Coxiella burnetii


  • Grows in cytoplasmic vacuoles
  • Stimulated by low pH of a phagolysosome
  • Resistant to host degradative enzymes
  • Endospore formation
  • Extremely resistant to heat and drying
  • Can persist outside host for long periods
  • Causes disease in livestock but not transmitted to humans by arthropods
• Transmission of Coxiella burnetii is made possible because of its ability to withstand drying
• Coxiella burnetii can also enter the body via other mucous membranes, abrasions, and the gastrointestinal tract through consumption of milk from infected animals
• Common signs and symptoms of Q fever


  • Sudden onset of high fever (104-105 F)
  • Headache
  • Malaise and fatigue
  • Nausea and/or vomiting
  • Chills and sweating
  • General feeling of sickness and loss of appetite
• More serious complications of Q fever can affect the immune-compromised, individuals with heart valve defects, and pregnant women
• Phase I (Virulent form)


  Present during Q fever
• Phase II (Avirulent form)


  Present during Q fever
• Acute stage of Q fever

  1. Cell mediate immunity (CMI) is high (subclinical)

  2. Cell mediate immunity is low (disease occurs)

  3. Symptoms, fever, flu-like appear 1-3 weeks

  4. Infection spreads to macrophage (they can grow in phagolysosome, alveoli)

  5. Inflammation

  6. Atypical pneumonia

  7. Blood or digestive

  8. Liver (may or may not cause hepatitis)
• Chronic stage of Q fever


  1. Antibodies of phase I and II increase

  2. Formation of immunocomplex

  3. Endocarditis

  4. Blood culture (Negative)
• The presence of atypical pneumonia with hepatitis indicates that the patient had Q fever
• C. burnetii reproduces in the respiratory tract and then (in the absence of treatment) is disseminated to other organs
• Classic Q fever is an interstitial pneumonitis (not unlike some viral or mycoplasmal illnesses) that may be complicated by hepatitis, myocarditis, or encephalitis
• C. burnetii should also be considered as a potential causative agent in culture-negative endocarditis
• Infections are usually self-limiting but, in rare instances (especially endocarditis), can become chronic
• Laboratory identification of Q fever


  1. Serologic assays (acute stage detects antiphase II ≥ 200, chronic stage detects antiphase I and II)

  2. Culture and molecular (low sensitivity)

  3. PCR
• One organism of Coxiella burnetii can cause infection
• Treatment of Q fever


  1. Acute stage: Tetracycline

  2. Chronic stage: Doxycycline with Ciprofloxacin