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Features of tertiary syphilis

-occurs in 1/3 of untreated patients after 5+ years
-syphilitic aortitis:progressive dilatation of aortic root and arch with valvular insufficiency and proximal aortic aneurysm (caused by endarteritis of the vasa vasorum)
-neurosyphilis: e.g. tabes dorsalis, general paresis, or can be asymptomatic
-benign tertiary syphilis: gummas form in bone, skin and mucus membranes as a result of delayed hypersensitivity; rare, seen mainly in AIDS patients now


Congenital syphilis

-transplacental transmission, most often during primary or secondary syphilis
-early: snuffles, desquamative rash
-late/tardive:syphilitis osteochondritis and periostitis with saddle nose and saber shins; fibrosis of liver and lungs
-classic triad of late congenital syphilis: eight nerve deafness, interstitial keratisis and Hutchinson teeth


Transmission of Borrelia burgdorferi

-transmitted from rodents to humans via Ixodes ticks


Stage 1 of lyme disease

-erythema chronicum migrans: erythematous skin lesion at the bite site, usually recovers in 4-12 weeks, sometimes accompanied by fever


Stage 2 (early disseminated) lyme disease

-spirochetes spread hematogenously and cause secondary skin lesions, migratory arthralgias, lymphadenopathy, cardiac arrhythmias (myocarditis and pericarditis) and meningitis


Stage 3 lyme disease

-chronic, debilitating arthritis
-mild to severe encephalitis and polyneuropathy


Pathogenesis of lyme disease

-mostly secondary to the immune response


Morphology of skin lesions in lyme disease

-edema and lymphoplasmacytic infiltrate


Clostridium perfringens

-release collagenase and hyaluronidase to break down ECM and tissues
-secrete 14 different toxins, including alpha toxin which degrades cell membranes and causes nerve sheath damage


C botulinum, C tetani

-release neurotoxins that cause paralysis
-botulinum toxin blocks vesicle fusion at the neuromuscular junction preventing neurotransmission, resulting in flaccid paralysis; respiratory paralysis causes death


C difficile

-releases toxin A that stimulates chemokine production, and toxin B that causes cytopathic effects (cytotoxin)


Features of ricketttsial infections

-cause typhus, rocky mountain spotted fever
-primarily infect vascular endothelial cells
-manifestations of disease primarily due to vascular leakage


Major cause of death in rocky mountain spotted fever

-non-cardiogenic pulmonary edema causing ARDS


What are pseudohyphae

-buds fail to detach producing elongated chains, as in candida albicans


Four types of mycoses

1) cutaneous/superficial (dermatophytes)
2) subcutaneous: involve skin and subcutis with rare systemic dissemintation
3) endemic: dimorphic fungi that cause serious disease in healthy individuals
4) opportunistic: life threatening illness in immunocompromised individuals



-meningoencephalitis in healthy people and opportunistic infections
-inhaled; present in soil and bird droppings
-5-10 micron yeasts with a thick gelatinous capsule that is mucicarmine and PAS positive



-airborne conidia, inhaled, which germinate into hyphae that invade tissues
-neutrophils are a major defense against aspergillus such that neutropenia is a risk factor for invasive aspergillosis
-aspergilloma: colonizing fungus in lung cavities with minimal or no tissue invasion
-invasive aspergillosis: immunosuppressed hosts, primarily in the lung but wide hematogenous spread with a tendency for angioinvasion
-5-10 micron thick septate hyphae with acute angle branching (40 degrees)


Life cycle of malaria

-sporozoite, the infectious stage, is present in female Anopheles mosquito salivary glands that invade liver cells upon injection into human
-replicated rapidly in hepatocytes and release merozoites with rupture of the hepatocyte
-merozoites bind to red cells and hydrolyze hemoglobin
-in the red cell, goes from trophozoite to schizont which release two merozoites


Host resistance to malaria

-hemoglobin mutations such as HbC and sickle cell trait
-immune responses including antibodies and specific T cells



-obligate intracellular parasite
-promastigote develops and lives in the sandfly vector and amastigote multiples intracellularly in host macrophages
-four types of infection: cutaneous, visceral, mucocutaneous and diffuse cutaneous
-parasites stain with Giemsa


Chagas disease

-Trypanosoma cruzi, intracellular protozoan
-lethal acute myocarditis with amastigotes causing myocyte swelling
-chronic chagas: dilated, large heart (dilated cardiomyopathy), often with conduction defects and mural thrombi that may embolize


Taenia solium (cystercercosis)

-scolex (head) with suckers and hooklets and flat segments (proglottids) that contain reproductive organs
-if eggs are ingested, the larvae hatch and penetrate the gut wall, causing hematogenous dissemination and encyst in organs including the brain resulting in convulsions and other neurologic features


Echinoccocus granulosus (hydatid disease)

-ingested, hatch in the duodenum and invade liver, lungs and bone



-transmitted by freshwater snails
-eggs carried by portal circulation to liver cause prominent inflammatory reactions and eventual cirrhosis
-S hematobium: inflammatory cystitis