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32 Cards in this Set
- Front
- Back
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CMV
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Hepatitis, interstitial pneumotitis, skin rash, failure to thrive: Perinatal infection
Monospot test is negative. Fever with lymphocytosis, lymphadenopathy, hepatomegaly. Most opportunistic pathogen in AIDS Resemble erythoblastosis Fetalis. Microcephaly, mental retardation, hearing loss |
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CMV morphology
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Owl eye appearance and Reed sternberg cells in Hodgkin Disease
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CMV diagnosis
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CMV antigen detection, viral culture, PCR-based detection of CMV DNA, excrete CMV in urine and saliva.
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West Nile Virus
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Loss of CCR5
Mild fever, headache, myalgia, Maculopapular rash, Meningitis, encephalitis Autopsy: Temporal and brain stem involved. Elderly at highest risk |
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West Nile Virus Diagnosis
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Serology, viral culture, PCR
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Mechanism of transmission of CMV
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TNSVI
Transplacental Peri and neonatal Saliva Venereal Iatrogenic |
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Pathogenis of CMV
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1. Infect dendritic cells
2. Downregulate MHC class I and II 3. Produce TNF receptor, IL-10, and MHC 1 4. Products of CMV can both activate and evade NK cells |
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Receptors of Measles
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CD46- inactivates C3 convertase
SLAM- T cell activation |
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Transmission of measles
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Respiratory droplets. Multiply in endothelial, epithelial, macrophage, dendritic and in lymphocytes.
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Clinical signs of measles
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1. Croup
2.. Diarrhea with protein losing enteropathy 3. Keratitis 4. Encephalitis 5. Hemorrhagic rashes- black measles |
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Immunity of measles
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B cell protect against re-infection.
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Morphology of measles
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Koplik spots- opening of stensen ducts
Warthin Finkeldey gaint cells- lymphoid organs, lungs, sputum |
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Rare complications of measles
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SSPE, cognitive decline, spasticity, seizure, gliosis, myelin degeneration
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Diagnosis of measles
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Detection of viral ag in nasal exudate and urinary sediment.
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Mumps has 2 surface glycoproteins
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1. Hemagglutinin and neuraminidase
2. cell fusion and cytolytic activities |
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Mumps (what organs)
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Hematogenous spread to salivary glands and then to testis, ovary, pancreas and CNS
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Morphology of Mumps
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1. Mumps Parotitis- enlarged, doughy glands, moist glistening due to edema.
2. Mumps orchitis- marked swelling due to edema, hemorrhage and inflammatory cells. 3. Pancreatis- parenchymal and fat necrosis 4. Mumps enchephalitis- focal demyelination 5 Aseptic meningitis- extrasalivary complications of umps. 6. Infract of testis. |
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Tuberculoid leprosy
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1. Paucibacillary (no bacilli)
2. Dry scaly skin lesion with loss of sensation 3. Erythematous flat lesion with elevated hypergimented margins. Depressed pale centers (indicate healing) 4. Asymmetric peripheral Nerve - ulcers, and autoampution of fingers and toes. 5. epitheliod granulomas. Granulomas are seen in Tuberculoid leprosy. TH-1 secrete IL-2 and IFN-gamma which makes granuloma |
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Lepromatous Leprosy
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1. Multibacillary- skin, pheripheral nerve, testis
2. Macular, papular and nodular lesions on face, ears, wrist, elbows, knees- symmetric 3. Skin lesion- hypoaesthetic and anesthetic 4. Nose lesion- bacilli laden discharge 5. Ulnar and pheripheral Nerve 6. Testis- sterility 7. Lymph node- T zone involvement- collection of bacilli filled foamy macrophage in paracortex 8. splenic red pulp and liver in advanced disease- Lipra cells. 9. In advanced cases, M. leprae present in sputum and blood 10. No granuloma 11. Ab may form but they are not protective to the host, instead they form immune complex with a leading to erythema nodosum, vasculitis, and glomerulonephritis. |
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Leprosy
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Caused by mycobacterium leprae
M. Leprae is an acid fast, obligate intracellular organism it infectts and is transmitted by armadillos Grows best at 32-34 degree Celsius Replicates in cool area of the body. |
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Virulence of Leprosy
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Based on cell wall properties, it has no toxins.
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Pathogenesis of leprosy
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Like TB, it has cell mediated immunity mainly the Th-1 cells producing IL-2 and IFN- gamma
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Virulence factor of Aspergillosis
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Mnemonics- EAATS
1. adhesin- conidia can bind to fibronectin, laminin, fibrinogen, complement. 2. Antioxidant defense- melanin, superoxide dismutase 3. Enzymes- phospholipases, proteases 4. Toxins- Restrictocin and mitogilllin- theses are ribotoxins which degrades mRNA and inhibit host cell protein synthesis Aflatoxxin- Aspergillus flavus- carcinogen causes p53 mutations- hepatocellular carcinoma 5. Sensitization to spores- allergic alveolitis and broncopulmonary aspergillosis. |
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Pathogenisis of Aspergillosis
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1. Air borne conidia and portal of entry are the lungs
2. Conidia germinate to hyphae- they invade tissue 3. Major Host defenses: Neutrophils and macrophages Alveloar macrophage- ingest and kill conidia Neutrophils- produces reactive O2 intermediates- kill hyphae. |
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Invasive Aspergillosis
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1. opportunistic infection
2. Primary lesion in the lung 3. Widespread hematogenous dissemination- involvement of heart, value, brain. 4. Lung: Target lesions 5. Sharply delineated rounded grey foci with hemorrhagic borders- Necrotizing pneumonia 6. Fruiting bodies are formed in lung cavities. Vascular invasion points to aspergillus. Leads to superimposed hemorrhage and infraction. 7. Rhinocerebral aspergillosis resembles mucor infections |
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Aspergilloma
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Fungus secondarily colonizes cavities in the lung which are already present due to other diseases such as TB, infract, lung abscesses, bronchiectasis
brown masses called "fungal balls" are seen lying free within cavities. Surronding sparse inflammation or chronic inflammtion with fibrosis are seen. Recurrent hemoptysis. |
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Aspergillosis
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Caused by Aspergillus fumigatus
Ubiquitous mold causes Allergic bronchopulmonary aspergillosis Serious illness in the immunocompromised: sinusitis, pneumonia, and invasive aspergillosis predisposing conditions: neutropenia and corticosteroid. Aspergillus fumigatus growns in moldy barely and malt. "A man who works in Brewery. |
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Canadida esophagitis
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Aids or hematolymphoid malignancy
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Candida Vaginitis
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Diabetes, pregnancy or those in long term antibiotics
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Invasive Candidiasis
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1. Chemo for acute leukemias (neutropenia) and other immunosuppresed like aids
Hematogenous dissemination can lead to absecesses in kidney, brain, liver and heart. Endocartitis, meningitis, endophthalmitis Candida endocartitis- prosthetic valve and IV drug abusers |
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Cutaneous Candidiasis
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1. Onychomycosis
2. Paronychia 3. Folliculitis 4. Intertrigo 5. Balanitis 6. Diaper rash |
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Immune response to candida
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Innate and T cell response.
1st line of defense: phagocytosis and oxidative killing by neutrophils and macrophage. Increased infection in patients with neutropenia, defect in NADPH oxidase and myeloperoxidase Yeast activates dendritic cells to produce IL-12 which elicits protective anti fungal TH1 response. Filamentous form can escape from phagosomes, enter cytoplasm, and proliferate there |
