Medical Pathophysiology Past Paper MT 25 (Lec) - Sinco - Topic 4 PDF

MEDICAL PATHOPHYSIOLOGY MT T E R M Mt 25 (LEC) \ SINCO, LEO TEOPHANE ‘24...

MEDICAL PATHOPHYSIOLOGY MT T E R M Mt 25 (LEC) \ SINCO, LEO TEOPHANE ‘24 ‘25 01 TOPIC IV: PATHOPHYSIOLOGY OF INFECTIOUS DISEASES BACTERIAL INFECTIONS OUTLINE TUBERCULOSIS I Bacterial Infections A Tuberculosis Tuberculosis B Syphilis II Viral Infections WHO: TB is estimated to affect more than 1 A EBV billion individuals worldwide B Herpes C CMV ○ 8.7 million new cases each year III Fungal Infections ○ 1.4 million deaths each year A Candidiasis Significant progress toward reduction of cases ○ Globally recorded between 2010 and 2011 ROUTES OF MICROBIAL INFECTION (compared to 1990): new cases fell at a rate of 2.2% Major Local Basis for Failure of Pathogens mortality has decreased by 41% Site Defense(s) Local Defense (examples) In most healthy people, primary tuberculosis is asymptomatic, although it may cause fever Skin Epidermal Mechanical defects S. aureus, barrier (punctures, burns, Candida albicans, and pleural effusion ulcers) Pseudomonas aeruginosa ○ Fibrocalcific pulmonary nodule Needle sticks HIV, hepatitis tiny; at the site of infection viruses only evidence of infection if any remains Arthropod and animal Yellow fever, bites plague, Lyme Course of Infection disease, malaria rabies Infection typically leads to the development of Direct penetration Schistosoma delayed hypersensitivity to M. tuberculosis antigens GI Tract Epithelial Attachment and local Vibrio cholerae, barrier proliferation of Giardia ○ Can be detected by the tuberculin (PPD, or microbes Mantoux) skin test Attachment and local Shigella, POSITIVE: T-cell-mediated immunity to invasion of microbes Salmonella, Campylobacter mycobacterial antigens but does not Uptake through M cells Poliovirus, certain differentiate between infection and active pathogenic bacteria disease Acid Acid-resistant cysts Many protozoa FALSE-NEGATIVE: may occur in the secretion and eggs and helminths setting of certain viral infections, Bile and Resistant microbial Hepatitis A, sarcoidosis, malnutrition pancreatic external coats rotavirus, enzymes Norovirus FALSE-POSITIVE: may result from Normal Broad spectrum Clostridium difficile infection by atypical mycobacteria or prior protective antibiotic use vaccination with BCG (Bacillus flora Calmette-Guerin), an attenuated strain of Respiratory Mucociliary Attachment and local Influenza viruses M. bovis that is used as a vaccine in Tract clearance proliferation of microbes some countries Ciliary paralysis by Haemophilus toxins influenzae, M. Pathophysiology pneumoniae, Bordetella pertussis Resident Resistance to killing by M. tuberculosis alveolar phagocytes macrophage Urogenital Urination Obstruction, microbial E. coli Tract attachment and local proliferation Normal Antibiotic use Candida albicans vaginal floral Intact Microbial attachment N. gonococcus epidermal / and local proliferation epithelial Direct Infection/local Herpes viruses, barrier invasion syphilis Local trauma Various sexually transmitted diseases, e.g., human papilloma virus TENORIO | BSMT III 1  TOPIC IV: PATHOPHYSIOLOGY OF INFECTIOUS DISEASES NOTES May ensue in older adults and High effectivity (of mycobacterium) due to age & immunosuppressed people immunocompromised status The apical lesion expands into adjacent lung and eventually Progressive erodes into bronchi and Stages of Infection Pulmonary vessels. TB This evacuates the caseous Form of disease that develops in center, creating a ragged, a previously unexposed and irregular cavity that is poorly therefore unsensitized, person walled off by fibrous tissue. (first encounter). Progressive primary Occurs when organisms draining tuberculosis through lymphatics enter the ○ more often resembles an acute venous blood and circulate bacterial pneumonia with back to the lung. consolidation of the lobe, hilar Miliary lesions adenopathy, and pleural ○ may expand and coalesce, effusion. resulting in consolidation of large regions or even whole Primary TB lobes of the lung. With progressive pulmonary tuberculosis, the pleural cavity is invariably involved, and may Miliary develop: Pulmonary ○ serous pleural effusions Disease ○ tuberculous empyema, or ○ obliterative fibrous pleuritis Figure: Primary pulmonary tuberculosis, Ghon complex. The gray-white parenchymal focus is under the pleura in the lower part of the upper lobe (red arrow). Hilar lymph nodes with caseation are seen on the left (blue arrow). The pattern of disease that arises in a previously sensitized host (reinfection). Figure: Miliary tuberculosis of the spleen. The cut May follow shortly after primary surface shows numerous gray-white tubercles. Secondary tuberculosis, but more commonly TB it appears many years after the initial infection, usually when host resistance is weakened. Most commonly stems from reactivation of a latent infection. Involves the apex of the upper lobes of one or both lungs Because of the preexistence of hypersensitivity, the bacilli elicit a prompt and marked tissue response that tends to wall off the focus of infection. As a result, the regional lymph nodes are less prominently Laboratory Diagnosis involved early in secondary The diagnosis of pulmonary disease is based in Secondary disease than they are in primary part on the history and on physical and Pulmonary tuberculosis. radiographic findings of consolidation or TB cavitation in the apices of the lungs. Acid-fast smears and cultures of the sputum of patients suspected of having tuberculosis should be performed. (must be active disease) Culture on solid agar media show growth at 3 to 6 weeks, but culture in liquid media can provide an answer within 2 weeks. ○ PCR amplification of M. tuberculosis DNA allows for even more rapid diagnosis. ○ Culture remains the gold standard Figure: Secondary pulmonary tuberculosis. The upper parts of both lungs are riddled with gray-white areas of because it also allows testing of drug caseation and multiple areas of softening and susceptibility. cavitation. TENORIO | BSMT III 2  TOPIC IV: PATHOPHYSIOLOGY OF INFECTIOUS DISEASES Stages of the Disease ○ Culture media Ogawa Lasts for 1-6 weeks Middlebrook Endothelial skin thickening occurs Lowenstein-Jensen with the aggregation of lymphocytes, plasma cells, and Treatment & Management macrophages TB - DOTS (Department of Health) Appearance of a chancre Rifampicin & Isoniazid ○ Develops between 10-90 days ○ First line drugs post infection Amikacin, Kanamycin, or capreomycin ○ Painless, solitary lesion with Primary ○ Second line drugs raised and well-defined borders Stage ○ Antibodies produced 1-4 weeks ○ For Multidrug-Resistant Tuberculosis after appearance of chancre (MDR-TB) and Extensively Drug-resistant ○ If untreated may progress to Tuberculosis (XDR-TB) strains. secondary stage SYPHILIS Syphilis Venereal syphilis is a sexually-transmitted disease caused by a spirochete Great Pox; Evil Pox; Italian/French/Spanish Observed 1-2 months after the disease disappearance of primary chancre Earlier treatment was with the use of arsenic Systemic dissemination of the compounds but is now replaced by penicillin organism occurs (or doxycycline) Spontaneous healing occurs, as in the primary stage NOTES Serologic Tests now reactive Christopher Columbus (dark field microscopy) Brought TB & syphilis from old world → new If left untreated, 25% of cases of world primary syphilis will progress to Brought smallpox from new world → old world secondary syphilis Symptoms: ○ Generalized lymphadenopathy The Agent ○ Rashes in the skin and mucous Treponema pallidum membranes subspp. Pallidum (formerly ○ Malaise Spirochaeta pallida, 1905) ○ Fever Family: Spirochaetaceae ○ Pharyngitis Secondary ○ Early signs of neurologic Long, slender, helically Syphilis involvement (40%): visual coiled, gram-negative, disturbances, hearing loss, etc. microaerophilic bacteria Condyloma lata Possess endoflagella / ○ Painless, wart-like lesions axial filaments ○ Persist from a few days up to 8 Characteristic motility: corkscrew weeks followed by spontaneous Treponemal rare outer membrane proteins healing of the lesion as in (TROMPS) primary syphilis ○ Named for the outer phospholipid bilayer membrane which has very few exposed proteins thus delaying the host immune response Modes of Transmission Typical: Direct sexual transmission The organism is rapidly destroyed by: ○ Heat ○ Cold ○ Drying out General lack of clinical 30-50% transmission rate among individuals symptoms with active lesions Arbitrarily divided into two phases: Other potential MOT: ○ Early latent (infection is 1 year) ○ Parenteral exposure (rare) Patients at this stage are typically non-infectious ○ Exception: pregnant women who can transplacentally infect the TENORIO | BSMT III 3  TOPIC IV: PATHOPHYSIOLOGY OF INFECTIOUS DISEASES fetus even if they appear Liveborn infants often have no clinical signs of asymptomatic disease during the first few weeks of life Positive for serologic and Some may remain asymptomatic treponemal tests 60-90% develop later symptoms if not treated at birth Occurs in around one third of Signs & Symptoms untreated individuals ○ Necrotizing funisitis – Appears anywhere from months to inflammation of the umbilical cord; years after the secondary stage first indication of the disease ○ Often between 10-30 years ○ Hemorrhagic rhinitis Has three major manifestations: ○ Gummatous syphilis ○ Skin eruption – maculopapular ○ Cardiovascular disease rash around the mouth, palms, and soles ○ Neurosyphilis ○ Others: ————————————————— Generalized lymphadenopathy GUMMAS Hepatosplenomegaly Localized areas of Jaundice granulomatous Anemia inflammation on Painful limbs bones, skin, or Bone abnormalities subcutaneous Neurosyphilis tissue May heal Hutchinson’s Triad: spontaneously (but ○ Malformed teeth (Hutchinson with scars) or incisors and mulberry molars) become chronic inflammation ○ Interstitial Keratitis Contain: ○ 8th nerve deafness ○ Lymphocytes ○ Epithelioid cells Laboratory Diagnosis ○ Fibroblastic cells Represent the host’s response to the infection DIRECT DETECTION OF SPIROCHETES Resembles leprosy Tertiary Requires the presence of active lesions Syphilis Tests: Dark-field Microscopy & Fluorescent CARDIOVASCULAR COMPLICATIONS Antibody Testing Spirochetes appear to heave DARK FIELD Stages Detected: Primary and predilection for vasa vasorum of MICROSCOPY Secondary Syphilis the aorta Aortitis → dilation Involves detection of T. pallidum → valve in exudates from skin lesions incompetence → Collection site must be aneurysm cleansed prior to collection May result to Limitations & Errors angina pectoris ○ False Negative (severe chest pain) Delay in evaluating the slides NEUROSYPHILIS Insufficient specimen Complication Pretreatment with most often antibiotics associated in 3° ○ False Positive stage If specimen is obtained Can span all from the mouth or rectal stages of the area, morphologically disease identical nonpathogens ○ Often seen early in can be found. immunodeficient patients Late manifestations: NON-TREPONEMAL SEROLOGICAL TESTS ○ Tabes dorsalis - degeneration of the spinal cord Only used as Screening Tests ○ General paresis - chronic Detects for the presence of reagin progressive dementia ○ An antibody formed against cardiolipin (a lipid material from damaged cells) ○ May also be present in other disease states (nonspecific) Positive results are confirmed with more specific treponemal tests Congenital Syphilis Principle: Flocculation reactions ○ A specific type of precipitation that occurs over Occurs when a woman who has early syphilis a narrow range of antigen concentrations or early latent syphilis transmits treponemes to ○ Antigen consists of very fine particles the fetus Perinatal death: ~10% of cases TENORIO | BSMT III 4  TOPIC IV: PATHOPHYSIOLOGY OF INFECTIOUS DISEASES TREPONEMAL SEROLOGICAL TESTS NOTES Flocculation vs Agglutination Confirmatory tests Flocculation - fine clumps Detects antibody to T. pallidum antigens Agglutination - large clumps Testing: FTA-Abs, EIA, MHA-TP, DNA probe Antigen composition: FLUORESCENT One of the most used ○ Cholesterol – provides absorption centers TREPONEMAL confirmatory tests, an indirect and increases reacting surface ANTIBODY – fluorescent antibody test ○ Lecithin – neutralizes anti-C’ activity of ABSORPTION REITER’S STRAIN: cardiolipin (FTA-ABS) Non-pathologic strain of T. ○ Cardiolipin TEST pallidum Positive within 1-4 weeks after the appearance of NICHOL’S STRAIN: primary chancre Pathologic strain of T. Testing: VDRL, RPR pallidum VENEREAL Specimen: Heat inactivated DISEASE serum (56°C, 30 mins) or RESEARCH CSF LABORATORIES Principle: Flocculation (VDRL) TEST (precipitation with very fine particles) Reagent antigen: VDRL antigen ○ 0.03% cardiolipin – main reacting component ○ 0.9% cholesterol ○ 0.21% lecithin Rotation: 180 RPM (4 mins for serum, 8 mins for CSF) * ↑ Fluorescence = ↑ Organism Concentration Reporting: ○ Non-reactive: no clumps Grading/Reporting: ○ Weakly reactive: small clumps ○ Reactive: medium to large clumps False positive VDRL results: ○ SLE ○ RF ○ IM ○ Malaria TREPONEMA The standard test to which ○ Pregnancy PALLIDUM other treponemal tests are No heat inactivation necessary IMMOBILIZATION evaluated for CSF samples (TPI) TEST Best for CSF testing Best method to monitor therapy RAPID PLASMA Specimen: Serum REAGIN (RPR) Principle: Charcoal TEST agglutination * least performed test because of live T. pallidum from rabbit Reagent antigen: Modified VDRL antigen Interpretation (Bryant): ○ VDRL antigen + charcoal, EDTA, Thimerosal and Choline chloride (for chemical inactivation) Rotation 100 RPM (8 mins) Uses plastic cards HEMAGGLUTINA Reporting: May be qualitative or -TION TESTS quantitative Examined Macroscopically Reporting: ○ Non-reactive: no clumps ○ Weakly reactive: small black clumps ○ Reactive: medium to large black clumps NEWER TECHNOLOGIES IN SYPHILIS TESTING ENZYME Some EIAs have been IMMUNOASSAY developed to capture a TENORIO | BSMT III 5  TOPIC IV: PATHOPHYSIOLOGY OF INFECTIOUS DISEASES specific class of antibody to T. ○ amorphous tegument pallidum, either IgM or IgG ○ outer envelope Belong to the Herpesviridae family Referred to as the HHV-4 (Human Herpes Virus 4) Just like all other member of the Herpesviridae, EBV is capable of establishing latent infections in host cells Infectious Mononucleosis Affects the reticuloendothelial system A.K.A “The Kissing Disease” Infects: ○ CR2 (Complement Receptor 2)/CD21 cells (mostly B-cells) ○ squamous epithelial cells Incubation period: ○ 10–50 days or 4–7 weeks Mostly a self-limiting infection, but convalescence does not necessarily mean IMMUNOCHROM- A qualitative assay for the complete eradication of the virus from the body ATOGRAPHY detection of antibodies Infections among infants and young children against T. pallidum (IgM, are asymptomatic or mild IgG,or IgA) Adolescents and adults usually produce symptomatic illness (acute) Causes polyclonal activation of latently infected B-cells leading to production of several antibodies: ○ Heterophile antibodies – antibodies which cross–react with several antigens from different species (ex: sheep RBC Ags, Guinea Pig Kidney Ag, Bovine/beef RBC Ag) SOUTHERN Named after the discoverer: ○ EBV-specific antibodies – antibodies BLOT E.M. Southern directed to the different antigens of EBV. A.K.A. Southern ○ Auto-antibodies: Hybridization Assay Cold agglutinins Target DNA in sample is first Rheumatoid factors amplified through PCR ANA Involves isolating and amplifying a sequence of Signs and Symptoms DNA that is unique to a particular antigen. Common symptoms: The newly made DNA is then ○ sore throat subjected to agarose gel ○ fever electrophoresis using a ○ lymphadenopathy (lymphadenitis) technique known as Others symptoms: Southern blotting. ○ splenomegaly It has been applied to testing ○ hepatomegaly of various tissues (e.g. kidney, lymph nodes, eye, Symptoms last 2 – 4 weeks and skin), spinal fluid and Fatigue, myalgia, and need for sleep persists swab samples for the for months presence of treponemes. People with impaired immune systems progress to chronic active EBV infection, with life threatening IM associated symptoms. VIRAL INFECTIONS EPSTEIN-BARR VIRUS (EBV) Epstein-Barr Virus (EBV) Infection DNA virus large and complex in structure Composed of: ○ DNA core ○ protein capsid TENORIO | BSMT III 6  TOPIC IV: PATHOPHYSIOLOGY OF INFECTIOUS DISEASES Commonly observed among infected B-cells, but may also occur among SECs. The provirus does not express all of the genes, leading to production of incomplete viral antigens. Usually associated with EBNA. Established when the host DNA Latency polymerase acts on the genome of the virus instead of the viral DNA polymerase. For viral replication to occur, the viral DNA polymerase must copy the viral genome. Establishment of latency allows the virus to persist indefinitely in the body of the infected Laboratory Findings individual. Absolute lymphocytosis ○ >50 % of total leukocytes When stimulated, the latently infected host cell may shift to the ○ at least 10% Downey Cells, lytic cycle, initiating the enlarged lymphocytes with production of viral copies. atypical nuclei (scattered This is the reason some cytoplasm) previously infected patient shed Heterophile antibodies Reactivation virions in their saliva and other Antibodies to EBV antigens secretion and body fluids even if they are healthy. Burkitt’s Lymphoma In vivo reactivation is thought to A.K.A. ALL – III occur through stimulation of the latently infected B-cell receptor Lymphoproliferative disease of B-cells Starts with a tumor growing in the jaws or facial bones, but other sites may be affected. Primarily associated with children Common in Africa and Papua New Guinea Fatal if left untreated Other Malignancies Nasopharyngeal Carcinoma ○ Affects SECs ○ Common EBV-related malignancy in Southern China Gastric Carcinoma ○ CA of the stomach caused by EBV Post-transplant lymphoproliferative Epstein Barr Antigens disorder (PTLD) ○ Most common post-transplant malignancy EA – Early Antigen ○ Caused by reactivation or subsequent ○ produced during the initial stages of viral infection of EBV after organ transplant replication (Early acute phase) ○ Lymphoproliferation is noted Groups: ○ EBV DNA, RNA or protein can be detected in ○ EA-D – “diffuse” distribution in the nucleus tissue, further supporting evidence that the and cytoplasm virus is the culprit. ○ EA-R – “restricted” to the cytoplasm only VCA – viral capsid antigen Life Cycle of the EBV MA – membrane antigen ○ both are late phase antigens produced Production of virions from the following DNA synthesis infected host cell EBNA – EBV Nuclear Antigens Commonly observed among ○ appears in the latent phase infected SECs, where the viral ○ Types of EBNA: Lytic Cycle copies bud off from the host cell. EBNA-1 May also occur among infected EBNA-2 B-cells, but it usually occurs EBNA-3A through reactivation. EBNA-3B EBNA-3C EBNA-LP TENORIO | BSMT III 7  TOPIC IV: PATHOPHYSIOLOGY OF INFECTIOUS DISEASES LMP – Latent Membrane Proteins ○ Also a latent phase antigen ○ Types of LMP: LMP-1 LMP-2A LMP-2B Epstein Barr Antibodies Anti - Early Antigen (anti-EA) ○ Anti–EA-D IgG highly indicative of acute infection, first to appear and disappear 3 -6 months after infection ○ Anti–EA-R IgG Other Diagnostic Tests not usually found in young adults during the acute phase but may be seen in the Immunohistochemistry serum of very young children during the ○ Detects EBV Ags in tissue biopsies acute phase. ○ Useful for EBV-associated malignancies appears transiently in the later, Molecular Methods convalescent phase. ○ Detects EBV DNA in blood and tissue ○ In general, anti–EA-D and anti–EA-R IgG are samples not consistent indicators of the disease ○ Useful for patients with poor humoral stage. immune response Anti -Viral Capsid Antigen (anti-VCA) ○ Determines viral load in patient undergoing ○ Anti-VCA IgM therapy for EBV-associated malignancies usually detectable early in the course of CBC and Peripheral Blood Smears infection (INCUBATION PERIOD) ○ Absolute lymphocytosis with > 50% of the rise early in illness but is low in total WBCs concentration and disappears within 2 to 4 months. ○ At least 10% are atypical lymphocytes ○ Anti-VCA IgG HERPES SIMPLEX VIRUS usually detectable within 4 to 7 days after the onset of signs and symptoms Herpes Simplex Virus (HSV 1 and 2) persists for an extended period, perhaps lifelong. HSV-1 & HSV-2 differ serologically but are Anti- Epstein-Barr Nuclear Antigen closely related genetically and cause a similar (anti-EBNA) set of primary and recurrent infections. ○ Anti-EBNA IgG Both replicate in the skin and the mucous does not appear until a patient has membranes at the site of entry of the virus entered the convalescent period. (usually oropharynx or genitals), where they rise late in the infection and persist for life produce infectious virions and cause vesicular ○ Almost always present in sera containing lesions of the epidermis. IgG antibodies to VCA of EBV unless the Reactivation of HSV-1 and HSV-2 may occur patient is in the early acute phase of repeatedly with or without symptoms, and infectious mononucleosis. results in the spread of virus from the neurons ○ To establish a diagnosis, test results of to the skin or to mucous membranes. antibodies to EBNA should be evaluated in HSV-1 relation to: ○ the major infectious cause of corneal patient symptoms blindness in the United States. clinical history ○ Corneal epithelial disease is thought to be antibody response patterns to VCA and due to direct viral damage. EA HSV-2 ○ infection increases the risk of: HIV transmission by four-fold HIV acquisition by two to three-fold Pathophysiology HSV-1 and HSV-2 cause lesions ranging from self-limited cold sores and gingivostomatitis to life-threatening disseminated visceral infections and encephalitis. Gingivostomatitis ○ caused by HSV-1 ○ a vesicular eruption extending from the TENORIO | BSMT III 8  TOPIC IV: PATHOPHYSIOLOGY OF INFECTIOUS DISEASES tongue to the retropharynx and causing cervical lymphadenopathy CMV in Immunosuppressed Individuals ○ usually encountered in children ○ Immunocompromised individuals (e.g., Genital herpes transplant recipients, HIV infected ○ more often caused by individuals) are susceptible to severe CMV HSV-2 than by HSV-1 infection; these may be either primary ○ vesicles on the genital infections or reactivation of latent CMV. mucous membranes as ○ In all these settings, serious, even well as on the external life-threatening, disseminated CMV genitalia that are rapidly infections in immunosuppressed people converted into superficial ulcerations, primarily affect the lungs (pneumonitis) and rimmed by an inflammatory infiltrate. gastrointestinal tract (colitis). Treatment & Management Anti-HSV medications: ○ Acyclovir ○ Famciclovir ○ Valacyclovir Pain relievers taken orally, such as: Histopathology: Owl Cells ○ paracetamol or ibuprofen. Nonsteroidal anti-inflammatory drugs (NSAIDs) Treatment & Management Since viruses are self-limiting, medication is not Antiviral medications: needed if infection is not severe or chronic. ○ ganciclovir (GCV) or valganciclovir (VGC) CYTOMEGALOVIRUS (CMV) can be used to treat CMV infections Cytomegalovirus (CMV) FUNGAL INFECTIONS β-group herpesvirus CANDIDIASIS can produce a variety of disease manifestations, depending on the age of the Candidiasis host, and, more importantly, on the host’s Most Candida infections originate when the immune status. normal commensal flora breach the skin or Transmission of CMV can occur by several mucosal barriers. mechanisms, depending on the age group Candida spp. affected. These include the following: ○ The most frequent cause of human fungal ○ Transplacental transmission infections (usually C. albicans) from a newly acquired or primary ○ Residing normally in the infection in a mother who does not have skin protective antibodies (congenital CMV). mouth ○ Neonatal transmission gastrointestinal tract through cervical or vaginal secretions at vagina birth ○ Usually live as benign commensals and ○ Transmission through saliva seldom produce disease in healthy people during preschool years ○ Cause vaginitis and diaper rash. ○ Transmission by the genital route Susceptible to superficial candidiasis: the dominant mode after about 15 years ○ Individuals with diabetes of age ○ Burn patients Greatly associated with blood transfusion, ○ Individuals with indwelling intravenous lines alongside Hepatitis C or catheters Pathophysiology ○ Individuals undergoing peritoneal dialysis The ability of C. albicans to grow as biofilms The most common clinical also contributes to its capacity to cause manifestation of CMV disease (and high survival rate). infection in ○ Candida biofilms are microbial communities immunocompetent hosts consisting of mixtures of: beyond the neonatal yeast period: filamentous forms ○ Infectious mononucleosis-like illness fungal-derived extracellular matrix fever Highly contagious (direct human contact) atypical lymphocytosis 25-37°C - temperature optimal for fungi growth lymphadenopathy hepatitis marked by hepatomegaly and abnormal liver function tests TENORIO | BSMT III 9  TOPIC IV: PATHOPHYSIOLOGY OF INFECTIOUS DISEASES Pathophysiology Most commonly takes the form of a superficial infection on mucosal surfaces of the oral cavity (thrush) (common in HIV patients). ○ Florid proliferation of the fungi creates gray-white, dirty-looking pseudomembranes composed of matted organisms and inflammatory debris. Candida esophagitis ○ Commonly seen in AIDS patients and in those with hematolymphoid malignancies. Candida vaginitis ○ Common, especially in women who are diabetic, pregnant, or on oral contraceptive pills. ○ Usually associated with intense itching and a thick, curd-like discharge. Cutaneous candidiasis ○ Can present in many different forms, including: infection of the nail proper (onychomycosis) nail folds (paronychia) hair follicles (folliculitis) moist, intertriginous skin, such as armpits or webs of the fingers and toes (intertrigo), and penile skin (balanitis). Treatment & Management Candidiasis can be treated with oral azoles, such as: ○ Fluconazole Dosage: 100-400 mg/d until the patient improves. ○ Itraconazole Dosage: 200-600 mg/d until the patient improves. REFERENCES Notes from the discussion/learning mats by: LEO TEOPHANE SINCO, RMT, MLS (ASCPi), MPH Silliman University PowerPoint presentation: Lecture 4_2024- Pathophysiology of Infectious Diseases TRANSES ARE EXCLUSIVE TO ICLS STUDENTS ONLY. CONTENTS TRANSCRIBED HERE ARE WITHIN THE INTELLECTUAL PROPERTY OF THE UNIVERSITY. SHARING OF TRANSES OUTSIDE THE INSTITUTION IS CONSIDERED AS A BREACH OF ACADEMIC INTEGRITY AND IS SUBJECT TO LEGAL ACTION. PLEASE BE GUIDED. TENORIO | BSMT III 10