This document provides information on various bacterial causes of hematological infections. It discusses septicemia caused by both gram-negative and gram-positive bacteria. It also covers brucellosis caused by Brucella species, relapsing fever caused by Borrelia species, typhus caused by Rickettsia species, and ehrlichiosis caused by Ehrlichia species. For each infection, it describes the causative agent, transmission, pathogenesis, clinical features, diagnosis, treatment and prevention.

1. Debre Berhan University
College of Health Science
Department Of
Medical Laboratory Science
Topic: Bacterial causes of haematological infections
By
Tsegahun Asfaw.

2. 1. Septicemia, Sepsis, and Septic Shock
Septicemia/ Sepsis
• Is a potentially life-threatening infection in which large amounts
of multiplying bacteria are present in the blood. It is commonly
referred to as blood poisoning.
• Septicemia usually results from a focus of infection in the body,
e.g. UTI, Pneumonia.
Severe sepsis
– Decrease in blood pressure
Septic shock
– Low blood pressure cannot be controlled

3. • Gram-negative rods are usually implicated. Endotoxin causes the
symptoms associated with a severe drop in blood pressure.
• Staphlococcus aureus, a gram positive cocci, may cause a toxic
sepsis especially in dialysis patients due to Exotoxin.
• Puerperal sepsis begins as a uterine infection following childbirth
or abortion; it can progress to peritonitis or septicemia.
Streptococcus pyogenes is the most frequent cause.
• Puerperal sepsis/Childbirth fever – Streptococcus pyogenes:
Gram + cocci in uterus → abdominal cavity → blood →
septicemia
• Streptococcus agalactiae are a common cause of neonatal sepsis.

5. Pathogenesis
DIC
DIC

7. • Endotoxin stimulation of humoral and cellular immune
systems activation of complement sequence and coagulation
cascade.
• Complement activation chemotaxis of PMNs, degranulation
of mast cells, and release of histamine and inflammatory
mediators increased capillary permeability
• Inflammation release of catecholamines and prostaglandins
generalized vasoconstriction.
• Vasoconstriction decreased perfusion of vital organs
tissue hypoxia metabolic acidosis decreased cardiac
output

8. • Decreased cardiac output decreased coronary and cerebral
blood flow intractable hypotension, coma, multi-organ failure
DEATH
SEPTIC SHOCK CLINICAL MANIFESTATIONS
• Altered mental status
• Thermal instability
• Cardiac dysfunction
• Respiratory compromise
• Bleeding
• Jaundice
• Skin changes

9. Lymphangitits, a sign of sepsis. Note the clearly defined inflamed lymph vessels

10. 2. Brucellosis (Undulant Fever)
• causative agent: Brucella abortis (cattle), B. suis (swine), B.
melitensis (sheep and goats), and B. canis (dogs)
• Brucella is Small, Gram-negative coccobacilli; grows slowly
aerobically in the presence of carbon dioxide.
Method of transmission
• Direct contact with infected animals or their secretions on farms
or in slaughterhouses, consuming infected unpasteurized dairy
products, direct contact with skin abrasions, and through the
respiratory tract by way of aerosols.

11. Pathogenesis
• Brucella species are facultative intracellular pathogens that are
capable of surviving and replicating within phagocytic cells. Inside
the host, ingested by macrophages, multiply and move through the
lymphatic system into the bloodstream where they cause acute
bacteremia within 1 to 6 weeks.
• Cell wall lipopolysaccharide is the principal virulence factor
Clinical feature
• A gradual onset of symptoms occurs which includes a cyclic or
undulating fever that is high in the afternoon and low at night
after profuse sweating, fatigue, headache, and loss of appetite. The
bacteria may spread to the lymph nodes, liver, and spleen,
causing them to enlarge, and jaundice may result

12. Lab Dx
• Culture (takes 3-7 days): from blood, CSF and bone marrow
aspirate
• Serology to detect Abs against brucella
Prevention
• Eliminate infected animals from domestic herds
• Immunization of animal herds
• Pasteurize milk and dairy products
• Provide education and protective clothing for workers with
occupational exposure.
Treatment
• Tetracycline and streptomycin, gentamicin, or rifampin may be
added in severe cases.
• Prolonged treatment is necessary because the bacteria are in
macrophages and resistant to antibiotic .
• Recovery is usually spontaneous, but chronic aches and
nervousness may develop

13. 3. Relapsing fever and Lyme disease
• causative agnet: Borrelia spp
• Spiral bacteria; motile; non-capsulated;
• Non-sporing; require specialized media for culture; anaerobic or
microaerophilic
Epidemiology
• Epidemic Relapsing Fever is transmitted person-to-person via
human body louse (B. recurrentis)
– Occurs in Ethiopia, Rwanda, and the Andean foothills
• Endemic Relapsing Fever: Transmitted from rodents to humans
(Borrelia hermsii, B. turicatae, B.parkeri , B.doutenii)
• Found world wide except in Antarctica and Australia
• Lyme Disease: Transmitted by hard ticks from mice to humans
(B. burgdorferi sensu lato)
United states, Europe and Asia

15. • Pathogenesis: antigenic variation
Relapsing fever
• Clinical presentations of epidemic louse-borne and
endemic tick-borne relapsing fever are essentially
the same. However,
• A small, pruritic eschar may develop at the site of
the tick bite.
• After a 1-week incubation period, the disease is
heralded by the abrupt onset of shaking chills, fever,
muscle aches, and headache.
• Symptoms resolve after 3 to 7 days, when the
borreliae are cleared from the blood
• Splenomegaly and hepatomegaly are common.

16. • Bacteremia and fever return after a 1-week a febrile period.
• Symptoms are generally milder and last a shorter time during this
and subsequent febrile episodes.
• A single relapse may indicates epidemic louse-borne disease
• As many as 10 relapses may indicates endemic tick-borne disease.
• Relapses are explained by changes in the microorganisms"
antigens.
• The body’s immune response destroys most of the antigens, but a
few bacteria remain and have surface antigens the immune system
fails to recognize

17. • The bacteria multiply and cause a relapse. Each relapse reproduces
a new population of bacteria that have evaded the immune defense
mechanisms.
• The disease is particularly dangerous in pregnant women because
it can cross the placenta and infect the fetus.

18. Lyme disease
• Lyme disease begins as an early localized infection, progresses to
an early disseminated stage, and, if untreated, can progress to a
late manifestation stage.
• After an incubation period of 3 to 30 days, one or more skin
lesions typically develop at the site of the tick bite.
• The lesion (erythema migrans) begins as a small macule or
papule and then enlarges over the next few weeks, ultimately
covering an area ranging from 5 cm to more than 50 cm in
diameter
• The lesion typically has a flat, red border and central clearing as it
develops; however, erythema, vesicle formation, and central
necrosis can also be seen.
• The lesion fades and disappears within weeks, although new
transient lesions may subsequently appear.

19. • Hematogenous dissemination will occur in untreated patients
within days to weeks of the primary infection.
• Complications
– Arthritis (in 60% of untreated patients)
– 10% to 20% will develop neurologic manifestations (most
commonly facial nerve palsy);
– 5% will have cardiac complications (usually varying degrees
of atrioventricular block).

20. Life cycle of the tick of Lyme disease, usually involving deer and mice. Humans
become accidental hosts.

21. The common bull’s-eye rash of Lyme disease, that appears at
the site of the bite.

22. Erythema migrans rash on
the thigh
Bluish-red skin lesions characteristic
of late, disseminated manifestations
of Lyme borreliosis

23. Treatment and prevention
Lab Dx: Microscopy (for RF), serology and PCR (for lyme disease)
Appearance of Borrelia recurrentis in blood. Giemsa stain.
Tretment and Prevention
• Relapsing fever: TTC or erythromycin;
• Lyme disease: TTC, Penicillin, Amoxicillin, Ceftriaxone
• Use of Insecticides or repellents; protective wearing

24. 4. Typhus
• caused by Rickettsias spp.
• They are small, Gram-negative bacilli (0.2–1 µm in diameter)
• Obligate intracellular pathogens
• Utilize ATP from host cell
• Grow only in tissue culture
Epidemiology
• Rickettsial infections are zoonoses with a variety of animal
reservoirs and insect vectors.
Associated infections
• Epidemic or louse-borne typhus, murine typhus, scrub typhus and
spotted fevers.
• Rickettsial infections are characterized by fever, headache,
malaise, prostration, skin rash, and enlargement of the spleen and
liver.

25. Species Principal
host/reservoir
Vector Disease
R. typhi Rats Fleas Murine typhus
R. prowazekii Humans/squirrels Lice Epidemic or Louse-
borne typhus
R.
tsutsugamush
i
Rats Mites Scrub typhus
R. akari Mice Mites Rickettsial pox
R. rickettsiia Dogs Ticks Rocky mountain
spotted fever
Vectors and infections associated with Rickettsia

26. . Typhus Group
1. Epidemic typhus (Rickettsia prowazekii)
• In epidemic typhus, systemic infection and prostration are
severe, and fever lasts for about 2 weeks.
• The disease is more severe and more often fatal in patients older
than 40 years of age.
• During epidemics, the case fatality rate has been 6–30%.
• 2. Endemic typhus or murine typhus (Rickettsia typhi)
• The clinical picture of endemic typhus has many features in
common with that of epidemic typhus, but the disease is milder
and is rarely fatal except in elderly patients.

27. Spotted Fever Group
• The spotted fever group resembles typhus clinically; however,
unlike the rash in other rickettsial diseases, the rash of the
spotted fever group usually appears first on the extremities,
moves centripetally, and involves the palms and soles.
• In untreated Rocky Mountain spotted fever, it is usually much
greater in elderly persons (up to 50%) than in young adults or
children.

28. Traditional Group
• Rickettsial pox (Rickettsia akari) is a mild disease with a rash
resembling that of varicella.
• About 1 week before onset of fever, a firm red papule appears at the
site of the mite bite and develops into a deep-seated vesicle that in
turn forms a black eschar
Scrub Typhus Group (Orientia tsutsugamushi)
• This disease resembles epidemic typhus clinically.
• One feature is the eschar, the punched-out ulcer covered with a
blackened scab that indicates the location of the mite bite.
• Generalized lymphadenopathy and lymphocytosis are common.
• Cardiac and cerebral involvement may be severe.

29. Lab diagnosis
• Serology: Weil–Felix test; immunofluorescence assays and ELISA
Treatment and Prevention
• Treatment is with tetracycline or chloramphenicol
• Infection can be prevented by avoidance of the various vectors
• Vaccination: A vaccine to R. prowazekii is available.

30. 5. Ehrlichia
• Ehrlichia: tiny (0.2-2 µm) gram-negative organisms that resemble
Rickettsia, divide by binary fission and multiply within the
cytoplasm of infected white blood cells.
• They are obligate intracytoplasmic bacteria that infect
mononuclear cells and granulocytes.
• Ehrlichiosis is affects various mammals, including mice, cattle,
dogs, deer, horses, sheep, goats, and humans.

31. Pathophysiology of ehrlichiosis
• Not completely understood.
• Like Rickettsia spp, Ehrlichia organisms gain access to the blood
via a bite from an infected tick
• Amblyomma americanum is the principle tick vector of E
chaffeensis and is the primary vector of human monocytic
ehrlichiosis
Diseases
• Human monocytic ehrlichiosis (HME)
• Human granulocytic ehrlichiosis (HGE).

32. • Emerging disease - is similar to RMSF and can be severe and life-
threatening.
• The most common symptoms are sudden high fever, tiredness,
major muscle aches, severe headache, and, in some cases, a rash.
Diagnosis
• Diagnosis is difficult because diagnostic tests are not widely
available
• The diagnosis of ehrlichiosis is usually based on symptoms and a
history of exposure to ticks.
Treatment
• Antibiotics

33. Thank you