Medical Micro 4th Year Others & Fungi PDF

Session 6 Others DNA Pharmaceutical Micro Others& Fungi Micro 3: 4th Year Others Bacteria. 1-Gram negative spira...

Session 6 Others DNA Pharmaceutical Micro Others& Fungi Micro 3: 4th Year Others Bacteria. 1-Gram negative spirals: Spirochetes Miscellaneous: 2- Mycobacteria 3. Mycoplasma 4. Rickettsia 5. Chlamydia 1- Spirochaetes Morphology: Long, thin-walled, flexible, G-ve spirals (spring shape), Axial filament “flagella” propelling the cell in a corkscrew-like enables spirochete to penetrate and invade host General Characteristics Spirochaetes are only seen by:  dark field microscopy  immunofluorescence silver impregnation Poorly stained by Gram-stain since they are very thin rods Some species are parasitic, some are free-living or part of the normal microbiome of humans and animals Human Pathogenic Spirochete 1. Treponema pallidum: causes Syphilis 2. Borrelia spp.: a) Borrelia recurrentis: Relapsing Fever b) Borrelia burgdorferi: Lyme Disease 3. Leptospira interrogans: Leptospirosis 1. Treponema pallidum: causes Syphilis - Obligate parasite slow-growing in host tissues - Cannot be grown on media due to its complex nutritional requirement & sensitivity to environmental factors Transmission & Epidemiology Acquired (venereal/STD): sexual transimitied dieseas *Transmitted from infectious lesions of skin (e.g., genitalia) to other persons by intimate contact. *The bacteria pass through broken skin carried by the blood stream to every organ in the body. Congenital: Transmitted transplacentally from pregnant women to their fetuses. Blood Transfusion: Collected during early syphilis. Pathogenesis and Clinical Findings No significant toxins or enzymes are produced Adherence to host cells through outer membrane proteins corkscrewing motility facilitates penetration and dissemination of the organism to host cells and blood vessels The spirochete coats itself with human fibronectin for protection from phagocytosis. WBCs Immune Response to Syphilis Antibodies to the organism are produced but do NOT stop the progression of the disease. Patients with early syphilis who treated can contract syphilis again. Patients with late syphilis are relatively resistant to reinfection. igG Others 1 Micro 3: 4th Year 4 Stages of Acquired Syphilis This is the most infectious stage of the disease. The spirochaetes multiply at the site of inoculation causing a local, hard painless ulcer 1. Primary Stage “chancre” on genital organs, lips following an asymptomatic period of 10-90 days. The ulcer heals spontaneouslyhighly infectiousmay spread to blood. 1-3 months after an asymptomatic period Secondary lesions may appear as a red maculopapular rash (palms and soles) 2. Secondary Stage Moist papules on skin ulcerate on the genitals “condyloma lata”. Lesions are rich in spirochaetes and highly infectious, but heal spontaneously. If not treated, the disease progresses to the latent & tertiary stage 1/3 of cases progress to the latent period “No visible signs or symptoms” can be divided into: 3. Latent a. Early latent period: infection occurred within the last 12 months “Hidden” Stage b. Late latent period: infection occurred more than 12 months ago Granulomatous lesions, nodules “Gummas” especially of skin and bones Lesions result from hypersensitivity reactions & can be extremely disfiguring 4. Tertiary Stage This stage may be fatal due to CNS involvement and brain or cardiovascular damage In tertiary lesions, treponemes are rarely seen Congenital Syphilis: Transplacental spread of T. pallidum after the 3rd month of pregnancy may result in: Fetal death “Still-birth” Prematurity Infected infants who survivedevelop a condition similar to secondary syphilis. Enlargement of the liver, spleen and lymph nodes is most common, brain damage, bone lesions occur. leaves residual characteristic signs e.g. Hutchinson's teeth and saddle nose. Lab Diagnosis  Clinical manifestations of syphilis Microscopy: During 1ry & 2ry stages spirochaetes demonstrated in early lesions by dark field or immunofluorescence microscopy Non-specific serologic tests Specific Serologic Test “Flocculation Tests” “standard tests for syphilis; STS” a) Venereal Disease Research Laboratory (VDRL) b) Rapid Plasma Reagin (RPR) test Used for routine screening & use of nontreponemal involve the use of treponemal surface antigens: carbon coated cardiolipin proteins as Ag React with Reagin: non-specific antibodies (IgG and Abs ++ within 2-3 weeks of IgM) in serum of the patients infectiontests are positive in most These antibodies are detectable in most cases of patients with primary syphilis. primary and secondary syphilis Advantages Results usually become negative after treatment & Positive for life should be used to determine the response to treatment Disadvantages False +ve reactions occur in infections such as malaria, i) Remain positive after effective leprosy, measles, hepatitis, infectious mononucleosis & treatmentcannot be used to determine autoimmune diseases. the response to treatment or reinfection. +ve results have to be confirmed by specific tests. ii) Cannot be used as screening procedures as they are more expensive & ++ difficult to perform than non specific tests Others 2 Micro 3: 4th Year 2- Borrelia spp. These species are maintained in enzootic cycles Their presence in humans and domestic animals Transmitted by arthropods (vector-borne disease) The epidemiology of Borrelia spp. is generally related to the life cycle of their vectors Cause 2 major diseases: Relapsing fever  Lyme disease Relapsing Fever Caused by: 1. Borrelia recurrentis 2. Borrelia duttoni Antigenic variation: the M.o. can change its surface protein antigens during the course of a single infection As antibodies develop against only one antigen, distinct variants produce relapses of the illness Repeated 3-10 times until occurrence of ultimate recovery associated with presence of Abs against several antigenic variants. Transmission & Epidemiology: 1) Endemic tick-borne relapsing fever: 2) Epidemic louse-borne relapsing fever: Caused by B. duttoni Caused by B. recurrentis Rodents & other small animals are the main reservoirs Humans are the only hosts transmitted to humans by soft ticks saliva transmitted from person to person by the human body louse (Pediculus humanus). The disease occurs mainly in Africa The disease occurs in poor living conditions in developing countries. Short febrile phases & several relapses Longer febrile periods and fewer relapses Pathogenesis & Clinical Findings 1. Arthropod bite introduces spirochaetes into the body. 2. Spirochaetes multiply in blood sudden attack of high fever “febrile period” muscles pain last for 3-5 days 3. followed by “afebrile” (no fever) period for 4-10 days followed by a recurrence of initial symptoms 4. During febrile period, the spirochetes are found in blood while sequestered in tissues during afebrile period. 5. There are from 3 -10 recurrences of diminishing severity. Lab Diagnosis 1. Stain: Giemsa stain 2. Molecular Techniques: PCR Prevention & Treatment Avoidance of arthropod vectors is the best means of prevention No vaccine is available due to antigenic variation of surface proteins. Tetracycline is the drug of choice. Others 3 Micro 3: 4th Year Lyme Disease Caused by Borrelia burgdorferi It is a zoonotic, vector- borne disease transmitted by black-tick (Deer Tick) bite Humans are “Accidental Hosts” High incidence in summer and predominant in North America The researchers isolated and identified B. burgdorferi from Egyptian animal breeds. They also found antibodies to the bacteria in human contacts who were suffering from fever of unknown origin. Lyme disease zoonosis in Egypt requiring investigation and ++ awareness-raising to  the risk of infection Pathogenesis & Clinical Findings: 3 Stages Early Localized Disease: circular, non pruritic, red rash “Bull’s eye” “Erythema migrans”: days to weeks Flu-like symptoms neurologic abnormalities present as meningitis, encephalitis, Early Disseminated Disease: cranial neuritis, neuropathy, ataxia, or facial palsy Several weeks to months - Heart palpitations “Lyme carditis” and meningitis Sporadic episodes of arthritis affecting large joints (i.e., knees) Late Disease: Chronic neurologic sequelae.: encephalopathy affecting memory, Months to years after infection mood, or sleep Short-term memory problems Lab Diagnosis Serologically by detecting IgM or IgG with “ELISA” PCR is used to detect B. burgdorferi DNA in many body fluids (joint fluids & CSF) Prevention & Treatment Avoidance of arthropod vectors is the best means of prevention. Treatment of choice for early lyme disease is doxycycline or amoxicillin For more severe forms or late lyme disease, ceftriaxone is more effective: especially in neurological sequelae. Post-treatment Lyme Disease Syndrome “PTLDS” - A term used to describe patients who have had well documented Lyme disease and who remain symptomatic for many months to years after completion of appropriate antibiotic therapy ”IDSA” - The patients suffer from non-specific symptoms (fatigue, widespread musculoskeletal pain, complaints of cognitive difficulties. - These patients are described as having post-treatment Lyme disease syndrome (PTLDS) or chronic Lyme disease - The cause of PTLDS is NOT known. Others 4 Micro 3: 4th Year Leptospirosis: Leptospira interrogans NOT stained with dyes but seen by darkfield microscopy Leptospirosis zoonotic disease Epidemiology Occupational Zoonotic: found in kidneys of rodents and domestic animals (dogs, cats, cattle, pigs) without causing any harmful effect (animal reservoirs)Animals excrete leptospiras in urinecontaminate water and soil. people who work in sewers are at high risk i.e. it is an occupational disease. Cases of leptospirosis can increase through contaminated water or use it for drinking or bathing & can increase after hurricanes or floods Pathogenesis & Transmission Swimming in contaminated  (M.o. enters the body through breaks in the skin) consuming contaminated food (vegetation) or drink can result in human infection. Outer membrane proteins are involved in the attachment to host tissues. Clinical Findings:: (Biphasic illness) 1st Phase : - Flu-like symptoms: 4-9 days: Fever, chills, muscle aches and headache 2nd Phase : characterized by damage of liver (jaundice, hemorrhage), kidneys (uremia) and CNS (meningitis) Combined renal and liver failure associated with leptospirosis is referred to as “Weil’s disease” Lab Diagnosis: based on history of exposure & clinical signs (fever, elevated bilirubin, elevated creatinine,….) - Serology: Rise in IgM agglutinating Ab by microagglutination or indirect hemagglutination test. - Molecular Testing: PCR Prevention & Treatment Avoiding contact with the contaminated environment Animal vaccination and eradication of rodents are important For patients with mild symptoms: Doxycycline is the drug of choice ceftriaxone are effective in severe cases 2-Mycobacteria The Antigenic Cell Wall Structure: Over 60% of the mycobacterial cell wall is lipid 1. Mycolic acids: lipid shell around the organism & affect permeability at the cell surface. - Prevent attack of the mycobacteria by cationic proteins, lysozyme, and oxygen radicals 2. Cord Factor Glycolipid (Treholase Dimycolate ,TDM) responsible for the serpentine cording. - toxic to mammalian cells and inhibitor of PMN migration. - most produced in virulent strains of MTB. Others 5 Micro 3: 4th Year 3. Protein fraction: major component of Freund's complete adjuvant (Ag+ + oil) to boost immune response. - Antigens in the purified protein derivative (PPD) is isolated from culture media filtrates of Mycobacterium tuberculosis used in skin test (tuberculin skin test, TST). Cell Wall Properties Impermeability to stains and dyes: Acid-fast Resistance to many antibiotics  Resistance to killing by acidic and alkaline compound Resistance to osmotic lysis by complement. Resistance to lethal oxidations & survival inside of macrophages Mycobacteria of medical importance Mycobacterium tuberculosis complex (M. tuberculosis and M. bovis)causes tuberculosis (T.B)Pandemic inf.  Mycobacterium leprae causes leprosy (Hansen disease)  Non tuberculous mycobacteria (NTM) cause pulmonary diseases resembling tuberculosis, skin disease, or disseminated disease eg: M. avium  Mycobacterium tuberculosis complex Predisposing Factors: - HIV infection  1st predisposing factor for MTB infection (25% cases) - Close contact - Poor nutrition - Alcoholism & smoking Transmission: 1. By aerosols created by coughing or sneezing 2. The mycobacteria are killed by ultraviolet (daylight)Transmission is usually indoors 3. Transmission of M. bovis occur due to drinking non-pasteurized infected milk causing intestinal tuberculosis Site of Infection: - Pulmonary TB: attacks the lungs (Most common) - Extra-pulmonary TB: affect the CNS, lymphatic, circulatory, genitourinary system, bones, joints and skin Death by TB: ++ death than any other single microbial agent due to: Increasing number of cases in developing countries (malnutrition, poor hygiene, housing conditions…) The emergence of multidrug resistant mycobacteria Increased incidence of immunocompromised patients and HIV infection Lack of development of new drugs for treatment Others 6 Micro 3: 4th Year Pathogenesis 1. Primary Infection:  Mycobacteria reach pulmonary alveoli replicate within a phagosome in alveolar macrophage.  produce a protein prevents the fusion of phagosome with lysosome “escape the degradative enzymes”.  This primary site of infection in the lungs is called the “Ghon focus” = 1ry lesion CMI help limiting the primary infection by the formation of granuloma (tubercle)  Granulomatous lesions consist of giant cells known as Langhans giant cells surrounded by of epithelioid cells, T-lymphocytes, B-lymphocytes then fibroblasts. 2. Secondary Infection: 10% of the cases 1. Caused by HIV, alcoholism, malnutrition, immunosuppression, old age… 2. Reactivation of the primary lesionT cells secrete cytokines and caseation of the granuloma “tuberculoma” 3. Spread occurs through the bloodstream to the more distant tissues where secondary TB lesions can develop in lung “transmissible”, peripheral lymph nodes, kidneys, brain, and bones. Clinical Symptoms - Unexplained weight loss, loss of appetite, night sweats, fever and fatigue “Consumption” - If TB disease is in the lungs: persistent cough, hemoptysis (coughing up blood) and chest pain. - If TB disease is in other parts of the body (extra-pulmonary)symptoms depend on the area affected. Others 7 Micro 3: 4th Year Laboratory Diagnosis: Direct methods: demonstration in the specimen. Specimen: From the site of infection: *sputum collected on 3 separate days (pulmonary) *CSF (meningitis) *feces (intestinal) * urine (urinary tract) * biopsy (bone or tissue). Stain: Acid-fast (Zeihl-Neelsen) stain of sputum. - The preferred method is flourescence microscopy  more sensitive than acid-fast staining. - Even if sputum is negative, tuberculosis is only excluded after negative cultures. Media: Lowenstein Jensen medium (enriched and selective) - incubated aerobically at 37°C for 2-4 weeks and for 6-8weeks to report negative growth. Animal pathogenicity: Inoculation of guinea pig to confirm virulence of the bacteria. DNA detection: PCR is used for rapid & direct detection.  Active TB: Chest X-ray Indirect Method: Mantoux Test = Tuberculin Skin Test or PPD Test 1. delayed type hypersensitivity used to detect CMI to tuberculosis 2. Positive 4-6 weeks after infection 3. Using a needle, 0.1 ml of PPD (purified protein derivative, tuberculin) is injected intradermally (middle forearm) 4. Produces a pale skin papulequickly disappears test is read after 72 hours. 5. +ve result indicates TB exposure (10 mm or more) False Positive/Negative Results False Positive: NTM infection Previous administration of BCG vaccine. Recent TB infection (less than 8–10 weeks) False Negative: Corticosteroid therapy Immunologically compromised persons IGRA: QuantiFeron-TB Gold: Blood test that quantitates the amount of IFN -γ produced in response to the 2 antigens from Mycobacterium tuberculosis which are distinguishable from those present in BCG and NTM. If the patient is infected with TB, their WBCs will release IFN-γ in response to contact with the TB antigens (analyzed by ELISA) TB -Sensitive Treatment For active T.B, if the organism is known to be fully sensitive: ❖ first line drugs: isoniazid, rifampicin, and pyrazinamide and ethambutol are used for 2 months (intensive phase) followed by isoniazid and rifampicin for 4 months (continuation phase). For latent T.B: ❖ isoniazid for 6 months  the risk of reactivation of T.B in immunocompetent people Others 8 Micro 3: 4th Year MDR-TB Treatment: Multi-drug resistant TB (MDR-TB) TB resistant to isoniazid and rifampicin. *Treatment of MDR-TB is with Second-line drugs chosen in the following order (based on known sensitivities): 1. Group A: Fluoroquinolones 2. Group B: Injectable Aminoglycosides. 3. Group C: Thioamides, oxazolidinones 4. Group D: nicotinamide analogues, isonicotinic acid. XDR-TB Treatment: - Extensively Drug Resistant (XDR-TB) is defined as MDR-TB that is resistant to Fluroquinolones & to one of Aminoglycosides - The period of treatment is long, since mycobacteria divide slowly metabolically inactive. - The necessity to use combined therapy at least 4 drugs o be effective are used concurrently. Prevention: Persons with TB and their contacts are identified and treated. Pasteurization of milk and destruction of infected cattle are important in preventing intestinal tuberculosis.  BCG (Bacille Calmette Guérin) vaccine: - BCG consists of a live attenuated strain derived from Mycobacterium bovisgenetically identical with the human type. - given to children in the 1st month & to adults exposed to infection after negative tuberculin test TB and Shisha The WHO regional office in Cairo estimates that 17% of TB cases are attributable to Water Pipe Smoking (WPS) (Shisha) even if plastic mouth part is changed. Leprosy: Mycobacterium leprae (Hansen’s Disease) Obligate intracellular parasitelacks many necessary genes for independent survival It grows very slowly (generation time= 14 days)average incubation period is 1 year & up to 20 years. The optimal temperature for growth (30°C) is lower than body temperaturegrows preferentially in the skin, nose, eyes and superficial nerves. Transmission: Prolonged close contact with patients with lepromatous leprosy, who discharge M. leprae in large numbers in nasal secretions & from skin lesions. Besides humans, armadillo & chimpanzees are able to contract leprosy. Bacterium can be grown in the laboratory by injection into mice it cannot be grown on artificial mediaas organism replicates I.C within skin histiocytes, endothelial cells & cutaneous nerve cell Others 9 Micro 3: 4th Year Types of leprosy: person’s immune response to the disease determine their type of leprosy Genetic factors may play a role in developing the disease, due to the observation of clustering of leprosy around certain families men (93%) are affected more than women (7%) If left untreated, leprosy can be progressivepermanent damage to the skin, nerves, limbs, and eyes. The disfiguring appearance of the disease is due to several factors: The skin anesthesia results in traumasbecome infected Resorption of bone loss of features such as the nose and fingertips  Infiltration of the skin & nerves leads to thickening & folding of the skin Treatment: - Leprosy is a curable disease and treatment provided in the early stage. - Dapsone with rifampin is used to treat tuberculoid form of disease - Clofozamine is added for the treatment of lepromatous form. - Treatment is given for at least 2 years or until the lesions are free of organisms. Prevention Isolation of all lepromatous patients Treatment of infected cases  Chemoprophylaxis with dapsone for exposed children  No vaccine is available, but BCG vaccination provides partial protection. Others 10 Micro 3: 4th Year Miscellaneous: 3. Mycoplasma 4. Rickettsia 5. Chlamydia 3-Mycoplasma General Characters - The smallest free-living, wall-less organisms - First thought a virus or fungus so named “mycoplasma’ = “fungus-formed” - Absence of cell wall: stain poorly with Gram stain not affected by antibiotics (penicillin and cephalosporins)inhibit cell wall synthesis - Their outer surface is a flexible 3 layer cell membranevariety of shapes. - Their bacterial membrane contains cholesterol. - Mycoplasmas is an obligate parasite. - Mycoplasmas can cause RNA & DNA mutation of the host cells cancer Lab Diagnosis: Grown in the Lab on artificial media, they have complex nutritional requirements. They grow slowly and require at least 1 week to form a visible colony.  The colony has a characteristic “fried-egg” shape. Mycoplasma pneumoniae It causes atypical pneumonia & transmitted by respiratory droplets attaches to host cells with a tiny arm coated in protein Antibiotics like tetracycline "protein synthesis inhibitors" used against mycoplasma infections Pathogenesis *Attachment sites include the upper and lower respiratory tractpharyngitis, bronchitis & pneumonia. *The respiratory mucosa is NOT invaded, but ciliary motion is inhibited & necrosis of the epithelium occurs. Immune Response Immunity to M. pneumoniae is incomplete & second episodes of disease can occur During M. pneumoniae infectionautoantibodies are produced against red cells “cold agglutinins”  extra-pulmonary manifestations: “Hemolytic anemia” Epidemiology +++ incidence in the winter. Frequent cause of pneumonia in young adults outbreaks “epidemics” in groups such as families and students. Sometimes called “Walking Pneumonia” as it spreads quickly in crowded areas & milder symptoms than other types of pneumonia. Clinical Findings Non-productive ‘dry’ cough, fever. The disease resolves spontaneously in 10-14 days. Others 11 Micro 3: 4th Year Mycoplasma pneumonia is the most common type of atypical pneumonia. The term "atypical" means:  causative bacterium cannot be isolated on routine media. The disease not resemble typical pneumonia (milder symptoms, prolonged course,  sputum production & extra-pulmonary symptoms) Lab Diagnosis Serology: “Cold agglutinin test” IgM autoantibodies against type O RBCs agglutinate at 4°C but not at 37°C. The test is non-specificfalse-positive results occur with influenza virus and adenovirus infections. Diagnosis can be confirmed. Sputum: Gram stain and culture are NOT helpful, except in excluding other pathogens Direct detection: using PCR or DNA probes. Treatment: choice is erythromycin, azithromycin or tetracycline. 4- Rickettsiae General Characteristics Obligate intracellular parasites Pleomorphic (cocci , rods or filamentous), single or in pairs, stained with Giemsa stain Grow only in tissue culture or yolk sac of embryonated eggs Rickettsial Groups: 2 gps The Typhus Group (TG) The Spotted Fever Group (SFG) - Louse-borne ”epidemic typhus”: with famine and war. - Tick-borne ”Rocky Mountain spotted fever” - Flea-borne ”endemic typhus” Organisms can be transmitted by: a. Bites of ectoparasites b. Inoculating infectious fluids or feces by the ectoparasites into the skin c. Inhaling infectious material cause infection for some of these organisms. Common Symptoms 1. Skin rash 2. Fever 3. Headache 4. Malaise 5. Hypotension 6. Acute renal failure 7. Respiratory distress Lab Diagnosis: Serology: Weil Felix Reaction - Non-specific microagglutination between serum of patient and antigens of Proteus vulgarisThis is due to the cross reactivity between the O-polysaccharide antigen of Proteus spp. & Ag found in many rickettsia Others 12 Micro 3: 4th Year Prevention & Control Avoidance of infected arthropods offers some protection Broad-spectrum antibiotics: doxycycline, tetracycline, and chloramphenicol. Q-fever: zoonotic , occupational disease -ve: Weil Felix Reaction 5- Chlamydiae General Characteristics: Obligate intracellular pathogens The most common bacterial sexually transmitted infection worldwide Rigid cell wall, stained by Giemsa stain They grow in tissue culture and in the yolk sac of chick embryo Biphasic life cycle: Alteration between 2 functionally & morphologically forms: Elementary Body “EB” Reticulate Body “RB” Infectious Non-infectious Metabolically inert Metabolically active “Binary Fission Once the EB enter the host cells, it reorganizes into a RBs begin a differentiation back to the infectious EBs, larger, metabolically active RB released from the host cell to initiate a new round of infection Others 13 Micro 3: 4th Year Chlamydiae of Medical Importance: Chlamydia trachomatis “STD” - causes the eye-disease trachoma & sexually transmitted infection chlamydia Chlamydophila pneumoniae: causes atypical pneumonia Chlamydophila psittaci: causes zoonotic infectious disease, psittacosis (pneumonia)parrot disease. “C. pneumonia and C.psittaci are sufficiently different molecularly from C. trachomatis that they have been reclassified into a new genus called Chlamydophila. Pathogenesis Chlamydia trachomatis Trachoma (chronic conjunctivitis): recur over many years lead to blindness but causes no systemic illness. Genital tract infection: occasionally transmitted to the eye or the respiratory tract In men: In women: causes non-gonococcal urethritisto epididymitis, Chlamydial cervicitis is characterized by: which in rare cases can cause sterility  Mucopurulent cervical discharge  develop pelvic inflammatory disease (PID) PID can cause scarring inside the reproductive organsinfertility or ectopic (tubal) pregnancy - Infants born to infected mothers often develop mucopurulent conjunctivitis one week after birth, may lead to blindness Ophthalmia neonatorum - Chlamydia may cause “reactive arthritis” especially in young men. The triad of conjunctivitis and urethritis and reactive arthritis is known as Reiter's Syndrome, which is an autoimmune disease caused by Ab formed against C. trachomatis cross reacting with antigens on the cells of the uveal tract, urethra and joints. Lab Diagnosis Specimen: from urine, urethra and cervix in genitourinary infections, conjunctivae in ocular disease and sputum in respiratory infections. Direct tests by detection of chlamydial DNA by PCR.  Culture: Chlamydiae can be grown in cell cultures Serologic tests: ELISA, immunofluorescence or complement fixation test. Treatment: - C. trachomatis infection can be effectively cured with: Tetracyclines as doxycycline & macrolides as erythromycin Others 14 Micro 3: 4th Year Fungi Characteristics: Eukaryotic. Cell wall contains polysaccharide Chitin. Cell membrane contains ergosterol  Fungi are obligate aerobes or facultative anaerobes Their habitat is environment, except Candida albicanshuman normal flora. Classified into: Unicellular e.g. yeast Multicellular e.g. molds & mushrooms Yeast reproduce by: Mold reproduce by:  Symmetrically by binary fission Binary fission Formation asexual spores or sexual spores. Asymmetrically by budding Asexual spores: sexual spores. 1. Haploid spores produced by 1. Mating between two haploid mitosis from a haploid spores forming a diploid spore parent cell. called a zygospore 2. Genetically identical 2. The zygospore is genetically to the parent cell different from the parents 3. Can develop into new haploid 3. The zygospore germinates, it individuals without being can undergo meiosis, fertilized forming haploid cells that develop into new hyphae Classification: According to morphology Others 15 Micro 3: 4th Year According to pathogenesis Pathogenesis: 1. Response to fungal infection is the formation of granulomas. A granuloma is a focal aggregate of immune cells that forms in response to a persistent inflammatory stimulus. - Granulomas produced in the systemic fungal diseases e.g. histoplasmosis & coccidioidomycosis & blastomycosis. 2. Fungi do not produce bacterial-type exotoxins & not have endotoxins in their cell walls. Intact skin is an affective host defense against certain fungi since: a. Fatty acids in the skin inhibit dermatophyte growth. b. Hormone-associated skin changes at puberty limit ringworm of the scalp caused by Trichophyton. c. Normal flora of skin   fungiwhen it is inhibited by antibioticsovergrowth of fungi such as Candida N.B: The mucous membranes of the nasopharynx is another defense systemtrap inhaled fungal spores Others 16 Micro 3: 4th Year Medically important Fungi Medical mycoses divided into 4 categories: Cutaneous Subcutaneous Systemic Opportunistic 1. Cutaneous mycoses Others 17 Micro 3: 4th Year 2. Subcutaneous mycoses 3- Systemic mycoses Others 18 Micro 3: 4th Year Others 19 Micro 3: 4th Year 4-Opportunistic mycoses Others 20