Medically Important Bacteria of Unique Morphology and Biology
• Rickettsia and Chlamydia - Strict intracellulairs - Gram negative coccobacilli ☻Mycoplasma - Cell wall deficient and highly pleomorphic
Rickettsiae • -
Three genera: Rickettsia (family rickettsiacea) Ehrlichia (family rickettsiacea) Coxiella (family rickettsiacea)
Vectors • Lice, ticks, fleas and transmission from human,rodents and insects. - Through blood infects The endothelial cells (Veins)
Morphology • Gram negative coccobacilli • Contain double layered cell wall • Giemsa staining is best method
Clinical study • Rocky mountain spotted fever (Montana) -Rickettsia rickettsi Wood tick and dog tick Transovarial transmission - Incubation period of 7 days - Fever, malaise, rashes in the extremities then spread generally. Complications : cardiovascular disorders and renal disorders.
• Children and adolescents most affected • Mortality rate in adults over 40 years is 5-30%
Louse born Typhus fever • Rickettsia prowazeki • Transmission is through louse from one person to another person. • The organisms are excreted through feces of louse .
Louse born Typhus fever • It is occurred in most populated areas with poor hygiene such as north of Africa • Incubation period is 8 days: - High fever,chills, sever headache,and mental disturbances. - Skin rashes sometimes develope - Continues for 2 weeks with sever symptoms in adults.
Louse born Typhus fever • Complications are included: mental disturbances and myocarditis • Mortality rate is 50%
Eschar of typhus
Diagnosis • Serologic test • Immunofluorescence methods • Cultivation on living cells and chicken embryo
Treatment • • • •
Tetracycline Doxycycline Chloramphenicol Anti louse shampoo or ointment
Prevention • Control of vectors • Adequate hygiene • Vaccines
Erlichia • Human erlichiosis • Tick born • Tow kind erlichiosis: -Human monocytic erlichiosis(HME) E.chaffeensis -Human granulocytic erlichiosis(HGE) E.Phagocytophila Morulae
HME
HGE
Clinical signs • • • • •
Acute fever Muscular pain Leukopenia Thrombocytopenia Some times result in death
Laboratory diagnosis • Antibody detection • PCR • Murolae in blood smear
Treatment • Doxycycline ( for 7-10 days)
Coxiella
Coxiella burnetii • Q.fever (Queensland, Australia) -These bacterial live in cytoplasmic vacoules of phagocytes and therefore resist to Phagolysosome action - Resist to heat and drying ,therefore live for longer times outside the body. - Produce diseases in livestocks( cattle)
- Transmission is not through insects - Transmission is by inhaling the polluted dusts in Butcheries and grain stocks.
Clinical studies • Primarily multiply in RS and without treatment spread to other organs • Interstitial pneumonia that complexes with myocarditis,hepatitis,or encephalitis. • Culture negative subacute endocardits (C.burnetii) • Usually self limited and mild that may progress to chronicity.
diagnosis • Serologic tests.
Treatment and prevention • Doxycyline • Vaccine used for persons of occupational exposure
Bartonella quintana • Causative agent of trench fever • First appeared in world war I • Since 1945 Cases occurred in endemic regions of Europe, Africa and Asia • Cycles between human and lice • But doesn’t kill lice and doesn't multiply intracellularly
Clinical symptoms • • • • • •
Include five to six day fever Leg pains Headache Chills Muscular aches The organism can persist in blood and responsible for later relapses
Bartonella henselae • • • -
Common agent of cat scratch disease(CSD) Infection connected to cat scratch or bite Clinical signs: Incubation period 1-2 weeks Cluster of small papules at the sight of inoculation - In a few days lymph nodes swelling and become pus filled
Lymph node swelling filled with pus
Bartonella henselae - Most infections remain localized and resolve in a few weeks. - Drugs such as tetracycline ,Erythromycin and Rifampin can be effective therapies - The disease can be prevented by through degerming of cat bite or scratch
Bartonella bacilliformis • • • • • • • •
Oroya fever Liver and spleen Destruction of RBC ( anemia) Sand fly transmission South America Blood smear diagnosis Antibiotics and blood transfusion Control of sand flies
Chlamydia
Chlamydia • Like rickettsia, chlamydia are obligate intracellular parasites that depend on certain constituents of host cells for growth and maintainence. • Gram negative cell wall • Pleomorphic.
Chlamydia • Chlamydia trachomatis: STDs,neonatal,ocular disease(trachoma). • Chlamydia pnemonia: Atypical pneumonia • Chlamydia psittaci: zoonosis of birds and mammals ( ornithosis in human).
Chlamydia forms • Two distinct stages: -Elementary body ( small metabolically inactive ,infectious form)released from infected host cell. -Reticulate body ( large noninfectious, actively dividing form)
C.trachomatis • Humans are pathogenic reservoirs • Often being carried with no symptoms. • Elementary bodies are transmitted by infectious secretions. • Disease is most sever in infants and children
C.trachomatis • Tow human strains: • - trachoma strain, which attacks the squamous cells of mucous membrane in the eye,GUT,and lungs • -lynmphogranuloma venerum, which invade the lymphatic tissues of the genitalia. -
Chlamydial disease of the eye • Ocular trachoma • Inclusion conjunctivitis
Ocular trachoma • OT affects the epithelial cells of the eye -major cause of blindness in certain parts of the world (Africa and Asia) -tranmission is favored by contaminated fingers,fomites,flies and hot dry climate.
Ocular trachoma • First signs;mild conjunctival exudate and slight inflammation of conjunctiva.followed by marked infiltraion of lymphocytes and macrophages into the infected area. • Rough appearance of inner layer of upper eyelid. • Vascular pseudomembrane of exudat and inflammatory leukocytes formed over the cornea(pannus) last few weeks and usually heals.
Ocular trachoma • • • •
Coplications: -corneal damage and impaired vision -secondary bacterial infection -deformation of tear ducts and eyelashes which predispose to dry eye and corneal abrasion
treatment • Early treatment with tetracycline or sulfa drugs is highly effective and prevents all of the complications.
Inclusion conjunctivitis • Usually acquired through contact with secretions of GUT. • Infantile conjuntivitis developes after 5-10 days passed through the birth canal of infected mother. • The most prevalent form of conjunctivitis( 100,000 cases per year)
Signs • Conjunctival irritation • Profuse adherent exudate,redness and swelling.
Inclusion conjunctivitis • Erythromycin and tetracycline must be instilled into the eyes • Most inclusion conjunctivitis in adults is seen with concurrent genital infections and appears to be from self inoculation or contamination. • Swimming pool water and shared towels. • The infection is similar to trachoma and can cause corneal scarring if untreated.
Sexually transmitted chlamydial disease • It is estimated that c.trachomatis is carried in the reproductive tract of 10% of all people. • With higher rate in promiscuous. • 70% of infected women harbor in the cervix are asymptomatic. • 10% of infected males show no signs.
pathogenicity • A syndrome of chlamydial infections in males is nongonococcal urethritis (NGU) • Women with chlamydial infection have cervicitis, accompanied by white drainage,endometritis and salpingitis (PID) • Sometimes complicated with gonococci, which makes the treatment difficult.
Sexually transmitted chlamydial disease • When a special strain of chlamydia chronically infects the GUT, the result is sever and disfiguring disease called LGV • The external genitalia,anus,rectum and inguinal lymphnodes are the typical targets of invasion.
Sexually transmitted chlamydial disease • Chlamydiae enter through tiny breaks in the perigenital skin or mucous membrane and form small painless vesicular lesions that escapes notice. • Symptoms are headache,fever and muscle aches . • The lymphnodes enlarge and become firm and tender.
Sexually transmitted chlamydial disease • The nodes can burst and heal with scarring that obstruct lymphatic channels. • Long term blockage of lymphatic drainage leads to chronic deforming edema of genitalia and anus.
Identification, treatment and prevention of chlamydiosis • Genital samples are taken with a swab inserted a few centimeters into the urethra or cervix,rotated and removed. • Most reliable diagnosis come from culture in chicken embryos,mice or tissue culture. • The most sensitive and specific test currently available are immunoflorescenc and PCR based probe.
• Methods useful in diagnosis of inclusion conjunctivitis are Giemsa or iodine stains
Treatment Urogenital chlamydial infections are treated with drugs that act intracellularly, such as tetrecyclines, erythromycin and rifampin. For prevention of the disease sexual partners of the patient should be treated, use of condom Routine ocular prophylaxis of newborns.
Chlamydia Psittaci and ornithosis • Psittacosis was adopted to describe a pneumonia like illness contracted with imported parrots and other psittacian birds in the last century. • New name was adopted as ornithosis. • Ornithosis is a world wide zoonosis that is carried latently in wild and domestic birds but become active in overcrowding conditions.
Chlamydia Psittaci and ornithosis • Infection is communicated to other birds,mamals and humans by contaminated feces and other discharges that become airborne and are inhaled.
Symptoms • Fever, chills, frontal headache,muscular aches,coughing and lung cosolidation. • Complications involving the meninges, brain, heart or liver. • Treatment is with tetracyclines or erythormycin • Recovery is often slow and fraught with relapses.
Control of the disease • Quarantining and giving antimicrobial therapy to imported birds.
Chlmydia pneumonia • Strict human pathogen • It has been linked to a type of respiratory illness that includes: pharyngitis, bronchitis, and pneumonitis • Mild illness in young adults. • More sever in asthmatic patients even causing death in this group.
• Mollicutes and other cell wall deficient bacteria (Mycoplasmas)
• • • • •
Self replicating microorganisms Cell wall deficient Tow clinical genus: -Mycoplasma Pneumoniae,M.hominis Ureaplasma urealyticum
Biological charcteristics • Pleomorphic 0.3-0.8µ • Not strict intracellular parasites and can grow on free cell media • Some of them are fastidious and needs sterols, fatty acids and preformed Purines and pyrimidines in media. • Bind tenaciously that normal defense mechanisms can not remove them • Cause chronic infections
• Animal mycoplasma are referred membrane parasites
Mycoplasma colonies on agar plate
Mycoplasma pneumoniae • Cause Primary atypical pneumoniae(PAP) • Different from penumococcal pneumoniae • PAP is also produced by riketssias, chlamydias, RSV,adenoviruses • Transmission is via aerosol droplets in persons in close contact( family, military,students, etc) • 3-10% of exposed persons are affected • Mortality rate is very low
Mycoplasma pneumoniae • Specific Receptors are in the respiratory epithelium. • Disturb the cilliary activities • Destroyes in2-3 weeks the cillia and epithelium and diffuse to other parts
Mycoplasma pneumoniae • Signs: fever, malaise, sorethroat, and headache Cough is in late stages and usually unproductive. Nasal symptoms Chest pain Ear ache
diagnosis • • • • • •
Cultivation for 2-3 weeks Patient history and signs Sputum smear is without bacteria WBC is normal Blisters in tympanic membrane Serologic test including CF,IF,IHA
treatment • Tetracyclines and erythromycine for 14-21 days
Other mycoplasma • M.hominis • Ureoplasma urealyticum Weak sexually transmitted pathogens Some times normal in vagina, urethra and cervix U.Urealyticum sometimes cause prostatitis, nongonococcal urethrithis
Other mycoplasma • Opportunistic in fetus infections causing miscarriage, still birth, premature birth and RTI • M.hominis: vaginitis, PID, kidney inflammation
Bacteria that have lost their cell walls
• L.forms or L-phase variants • Exposure to penicillins and enzymes(lysozyme) • Can even become stable and reproduce themselves that are not naturally related to mycoplasmas
• • • •
Group A streptococci Proteus Corynobacterium Mycobacterium
