SEMINAR1 Micro Para Review Template

SUBJECT:SEMINAR 1: MICROBIOLOGY & PARASITOLOGY Dr. Erwin Benedicto LECTURER: May 6, 2016 DATE: BATCH 2018 PARASITOLOGY Common Name Scientific Name Intestinal Nematodes Ascaris

Trichiuris

Hookworm Necator americanus

Infective Stage

Diagnostic Stage

Round worm / Giant Intestinal Round worm

Embroyanted egg

Adult: femaleprominent genital girdle Unfertilized Egg: coarse mammilated albuminous coating

Man

Whip worm

Embryonated eggs

Eggs in feces - Bipolar shaped with plug like translucent polar prominences Adult: male-360 caudal Egg: bipolar mucus plug - football

Man

Eggs in feces - Bluntly rounded with thin hyaline shell - Morula Adult: Semi-lunar cutting plate

Man

Hookworm

Filariform larva

Definitive Host

Intermediate Host (1o, 2o, etc) None

Clinical Presentation or Disease Ascariasis ● Lung infiltration ● Vague abdominal pain ● eosinophilia ● Severe colicky pain (biliary ascariasis) ● Ascaris pneumonitis ● Lactose intolerance and decreased growth rate in children

Flies, Rat

Trichuriasis ●

Abdominal

Pain ● Petechial hemorrhage ● Amebic dysentery ● Rectal prolapse ● Appecndicitis, granulomas

None

Uncinariasis ● Maculopapul ar lesions and localized erythema ● Ground itch/ dew itch ● Hookworm anemia d/t bleeding ● Papulovesicul ar eruption ● Bronchitis/pn

Prevention and Treatment ● Albendazol e 400 mg (DOC) singe dose ● Mebendazo le 500 mg single dose ● Pyrantel pamoate 10 mg/kg ● Ivermectin ● Sanitary disposal of human feces ● Health education ● Mass chemotherapy ● Mebendazo le 500 mg (DOC) ● Albendazol e 400 mg single dose ● Sanitary disposal of human feces ● Handwashi ng with soap and water ● Thorough washing & scalding of uncooked vegetables ● Health education Albendazole 400 mg (DOC), Mebendazole or Pyrantel pamoate ● ● Iron supplements ● Sanitary disposal of human feces ● Wearing of shoes or slippers

Scientific Name

Hookworm Ancyclostoma duodenale

Common Name

Old world hookworm

Infective Stage

Filariform larva

Diagnostic Stage

Egg: In morula Male: Tripartite dorsal ray Filariform larvabifid or notched end

PARASITOLOGY Definitive Host

Intermediate Host (1o, 2o, etc)

Man

---

Man

None

Strongyloides

Threadworm

Filariform larva

Enterobius

Pinworm, Seatworm, Oxyuris

Embryonated eggs

D-shaped eggs Lop-sided appearance; letter D

Man

None

Capillaria philippinensis

Pudok worm

L3 Larva

Eggs in feces - Peanutshaped with striated shells and flattened bipolar plugs

Man

Freshwater or brackish water fish

Clinical Presentation or Disease eumonia ● Diarrhea Wakana dse

Prevention and Treatment ● Health education Albendazole, Mebendazole or Pyrantel pamoate

● Anemia, constipation, cough diarrhea, eosinic pneumonitis ● Nausea, rashe in waist and buttocks ● Stomach ache, vomiting weigh loss ● Erythema and pruritic elevated hemorrhagic papules ● Lobar pneumonia ● Cochin China diarrhea (intractable, painless, intermittent diarrhea) ● Minute ulcerations or abscesses in cecal mucosa- upon attachment of the worm ● Perianal pruritus- upon egg desposition in the perianal area

● Albendazol e 400 mg x 3 days ● Ivermectin ● Thiabendaz ole 50 mg/kg ● Wearing of shoes and slippers ● Sanitary Disposal of human feces

Intestinal Capilliariasis ● Abdominal pain ● Chronic diarrhea ● Gurgling stomach ● Hypokalemia ● Severe protein-

● Mebendazo le 200 BID for 20 days (DOC) ● Albendazol e 400 mg OD ● Electrolyte

● Pyrantel pamoate 10 mg/kg (DOC) ● Albendazik e 400 mg ● Mebendazo le 500 mg ● Cleanliness and personal hygiene ● Handwashi ng ● Cut fingernails

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Scientific Name

Common Name

Infective Stage

Diagnostic Stage

PARASITOLOGY Definitive Host

Intermediate Host (1o, 2o, etc)

- Flat mucus plugs; coarsely pitted shells

Blood Nematodes Wucheria bancrofti

Bancroft’s filarial worm

3rd stage larva / L3 Filiform larvae

Sheated microfilaria

Man Lymphatics Bloodstream Peripheral Blood

Brugia malayi

Malayan filarial worm

3rd stage larva

Sheated

Man Lymphatics Peripheral bloodstream

Tissue Nematodes Trichenella spiralis

Trichina worm

Encysted larva

(+) larva in muscle biopsy

Pig Rat

● Culex fatigans ● Anopheles spp. ● Aedes spp. ● Mansonia spp

Mansonia spp. Aedes togoi Anopheles spp.

● Man

Clinical Presentation or Disease losing enteropathy ● fluid, protein and electrolyte malabsorption ● Weigh loss, malaise, anorexia, vomiting & edema ● Lymphedema ● Elephantiasis ● Hydrocele ● Filariasis Bancrofti; Bancroft’s Filariasis ● Wuchereriasis;

● Malayan filariasis ● Lymphedema ● Elephantiasis

Asymptomatic if light infections; Intestinal invasion with diarrhea, abdominal pain, vomiting; Larval migration to muscles: periorbital, facial edema, conjunctivitis, fever, myalgias, splinter hemorrhages, rashes, eosinophilia Myocarditis, CNS involvement,

Prevention and Treatment replacement ● High protein diet ● Avoid eating raw fish

● Diethylcarb amazine citate (DEC) 6mg/kg ● individuals ● Mosquito nets ● Insecticide use ● Albendazol e ● Surgical removal of elephantoid tissue; pressure bandaging ● Diethycarba mazine citrate (DEC) 3-6 mg/kg ● Personal preventive measures against mosquito bites Ivermectin Albendazole Surgical removal of elephantoid tissue ● Pressure bandaging ● Thiabendaz ole 25 mg/kg BID x 7 days ● Mebendazo le 20 mg/kg ● Bed rest ● Supportive treatment ● Cook meat thoroughly

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Scientific Name

Loa loa

Onchocerca volvolus

Dracunculus medinensis

Cestodes Taenia solium

Common Name

African Eye worm Loa worm Eye worm

Blinding filarial

Guinea Worm

Pork tapeworm

Infective Stage

Diagnostic Stage

L3 Filiform larvae

Sheated microfilaria

L3 Filiform larvae

Larva inside copepods

Cycticercus in muscle IS to 1st IH: (taeniasis solium & Cystercus cellulose) embryonated egg

Sheated microfilaria

Local lesion Worm/Larvae Calcifi qed Worms by x-ray

● Eggs in feces ● Gravid proglottid

PARASITOLOGY Definitive Host

Man Subcutaneous tissue

Man Subcutaneous tissue

Man - Mesenteric Tissues; migrate To lower ext

Man

Intermediate Host (1o, 2o, etc)

Chrysops dimidia and silacea (Mango-fly and day-biting fly)

Simulium spp. Black fly Buffalo gnat

Cyclops (copepods)

Taeniasis solium: Pig Cystercus cellulose: Man

Clinical Presentation or Disease pneumonitis ● Severe myalgia ● Periorbital edema ● Eosiophilia ● Difficulty chewing ● Extremity paralysis Calabar or fugitive swelling Hypersensitivity Migrating worm in subconjunctival tissue

Onchocerciasis Oncherial dermatitis Ocular manifestations ● Eosinophilia ● Urticaria ● Onchocercomata ● Photophobia ● Lacrimation ● Keratitis ● Blindness ● Blister with serous exudates ● Ulceration ● Pseudoperitoneal syndromes

● Mild nonspecific abdominal complaints ● Cycticercosis ● Neurocycticersosi s ● Retinal detachment ● Chorioretinitis

Prevention and Treatment ● Freezing of meat Analgesics Antipyretics

● mazine ● ● e ● ids ● ● mazine ● ● e

Diethylcaba Ivermectin Albendazol Corticostero Surgery Diethylcaba Ivermectin Albendazol

● Corticostero id ● Surgery ● Metronidaz ole ● Thiabendaz ole ● Provision of safe water supply ● Boiling water before drinking ● Discouragin g the use of step wells ● Praziquante l 5-10 mg/kg ● NIclosamid e ● Freezing at -20 C for 10 days to kill cycticercus ● Cycticercosi

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Scientific Name

Taenia saginata

Common Name

Beef tapeworm

Infective Stage

Cysticercus bovis in muscle of cattle IS to 1st IH: embryonated egg

Diagnostic Stage

●

Egg in

PARASITOLOGY Definitive Host

Intermediate Host (1o, 2o, etc)

Man

Cattle

feces ● Gravid proglottid

Diphyllobothrium latum

Fish / Broad tapeworm

Plerocercoid larva encysted in fish

Operculated eggs; Proglottids

Man Cats and Dogs

1st: Microcrustaceans (copepods) 2nd: Predator fish (walleye, pike, perch)

Echinococcus granulosus

Hydatid worm

IS to IH: embryonated egg IS to DH: hydatid cyst

Hydatid cyst in lungs, liver, brain

Dog Sheep

Man

Echinococcus multilocularis

Fox Tapeworm

Embryonated egg in feces

Hydatid cysts in liver, lungs, brain

Foxes Human: Accidental infection

Small Rodents

Hymenolepis nana

Dwarf tapeworm

IS to DH: embryonated egg

Embryonated eggs in feces

Man

Rice and flour beetle ( for indirect cycle) Man

Hymenolepis diminuta

Rat tapeworm

IS to IH: embryonated egg IS to DH: cystercoid larva

Eggs in stool Bilestained Fan

Man`

Rat

Clinical Presentation or Disease ● Autoinfection Irritation Intestinal disturbance ● Epigastric pain ● Perianal itching ● Weight loss ● Loss of appetite ● Hunger pangs Hyperchromic megaloblastic anemia Thrombocytopenia leukopenia

Toxic Mechanical ● Local immunosuppression ● Obstructive jaundice ● Eosinophilia ● Increased ICP ● Jacksonian epilepsy Alveolar hydatid disease Pain or discomfort in the upper abdominal region, weakness, and weight loss Slow growing, destructive tumor Irritation Small disturbances Autoinfection ● Headache ● Dizziness ● Restless ● Irritable ● Enteritis Irritation Intestinal disturbances Minimal and nonspecific

Prevention and Treatment s – Praziquantel 5075 mg/kg x 30 days Praziquantel 5-10 mg/kg

Praziquantel 5-10 mg/kg Freezing for 24 to 48 hours at T -18 C of fish All freshwater fishes should be thoroughly cooked Control the source of infection, proper disposal of sewage and marketing of fish Albendazole Surgical resection Health education Minimizing opportunities for transmission

Albendazole Surgery PAIR procedure

● Praziquante l 25 mg/kg ● Personal hygiene ● Environmen tal sanitation ● Proper storage of food ● Praziquante l 25 mg/kg single dose ● Rodent Page 5 of 33

Scientific Name

Common Name

Infective Stage

Diagnostic Stage

PARASITOLOGY Definitive Host

Intermediate Host (1o, 2o, etc)

Clinical Presentation or Disease

Dog flea Cat flea Human flea Dog louse

● Slight intestinal discomfort ● Epigastric pain ● Diarrhea

like hooklets Bipolar thickenings

Dipylidium caninum

Trematode Fasciola

Double-pored dog tapeworm

● Human fascioliasis ● Temperat e Liver fluke (Fasciola hepatica) ● Tropical liver fluke (Fasciola gigantica)

IS to IH: embryonated egg IS to DH: cystercoid larva

Egg in stool

Man

Metacercaria

Unembryonated egg in feces

Man

● ● ● ●

1 o – Lymnaea philippinensis (snail) - L. auricularia rubiginosa 2 o – Ipomea obscura(kangkong) - Nasturtium officinale

* Acute stage –larval migration and worm maturation in the hepatic tissue * Chronic stage –persistence of Fasciola worms in the biliary ducts, asymptomatic * Sudden onset of high fever, hepatomegaly and marked eosinophilia form a triad of diagnostic significance ● Fever ● Right upper quadrant abdominal pain ● Hypereosinophilia ● Biliary tract obstruction

Facsiolopsis buski

Giant Intestinal fluke

Metacercaria

Unembryonated egg in feces

Schistosoma

Blood fluke

Cercaria

Eggs in feces

● Pigs ● Man

Man

1 o– SNAIL (Segmentina or Hippeutis) 2 o – Aquatic plants (eg. Trapa bicornis/water caltrop, Eilocharis tuberose/water chestnut, Ipomea obscura/water morning glory, Nymphaea lotus/lotus);

Oncomelania hupensis/ Oncomelania quadrasi

Generalized toxic and allergic symptoms such as edema in face, abdominal wall and lower limbs *Profound intoxication can result in death ● Mucus secretion and minimal bleeding ● Intestinal obstruction ● Generalized toxic and allergic symptoms Granuloma formation leading to obstruction of the intrahepatic portal branches, Diarrhea, Meningoencephalitis,

Prevention and Treatment control ● Elimination of insect intermediate host ● Food protection Praziquantel 5-10 mg/kg Periodic deworming

● Bithionol 30-50 mg/kg ● Thorough washing or cooking of vegetables ● Boiling of water * Thorough washing or cooking of vegetable and boiling of water in areas of infection * Elimination of snail intermediate host and killing the parasite in the reservoir host by chemotherapy * Vaccination against Fasciola antigens ● Praziquante l 25 mg/kg ● Avoid soaking of aquatic plants in water ● Washing and boiling of plants

● Praziquante l ● Chemother apy

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Scientific Name

Common Name

Infective Stage

Diagnostic Stage

PARASITOLOGY Definitive Host

Intermediate Host (1o, 2o, etc)

Clonorchis

Chinese liver fluke

Embryonated egg

● Egg (biliary duodenal aspirate)

Man

1 o – Parafossarulus spp. (snail) and Bithynia spp. (snail) 2 o –Cryprinidae (fresh water fish)

Paragonimus westermani

Oriental Lung Fluke

Metacercaria In crustacean Cercaria w/ spines

Unembryonated egg in sputum or in feces if swallowed

Man

1 o - Antemelania asperata(snail) 2 o – Sundathelphusa philippina(crab)

Amebiasis

Quadrinucleate cyst

Protozoans Entamoeba histolytica

● Troph ozoites in liquid stools ● Cyst in formed stools

Clinical Presentation or Disease fever, lethargy and coma ● Dermatitis ● Superficial lung petechiae ● Pneumonitis ● Portal hypertension ● Ascites ● Hepatosplenomeg aly ● Cor pulmonale ● Motor/sensory disturbances * Intense proliferation of the biliary epithelium * Periductal fibrosis * Fatigue, weakness, weight loss, abdominal distress and altered appetite ● Cholagiocarcoma of the liver ● Impaired liver function but SGPT and SGOT are normal clinical manifestations consistent with pulmonary tuberculosis (PTB) ● Cough ● Rust-colored sputum with foul fish odor ● Chest pains ● Dyspnea ● Hemoptysis ● Granulomatous reaction of lungs

Man

● Flasklike primary ulcer ● Diarrhea with or without blood ● Ameboma ● Amebic Live Abscess extraintestinal amoebiasis Anchovy sauce Watery diarrhea; flask shaped

Prevention and Treatment ● Health education ● Control of oncomelania snails ● Environmen tal sanitation

● Praziquante l 25 mg/kg ● Treatment of positive cases ● Health education

● Praziquante l 25 mg/kg TID x 3 days(DOC) ● Bithionol 15-25 mg/kg BID ● Cook crabs sufficiently ● Health education

● Metronidaz ole (DOC) ● Asympto Diloxanide furoate and Metronidazole ● Amebic colitis – Tinidazole and Metronidazole ● ALA Tinidazole

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Scientific Name

Common Name

Entamoeba coli

Giardia lamblia

Trichomonas vaginalis

Leishmania tropica

Infective Stage Cyst

Giardiasis; Traveller’s diarrhea Gay bowel syndrome Lamblia duodenalis

Trichomoniasis

● Cutaneou s Leishmaniasis ● New World Cutaneous Leishmaniasis

Quadrinucleate cyst

Trophozoite

Promastigote

Diagnostic Stage

PARASITOLOGY Definitive Host

Trophozoite: dirty cytoplasm Cystic stage: Jagged or splintered end chromatoidal bodies Trophozoite: Ventral sucking disc (old man with eyeglasses) Cystic: Retracted cytoplasm with 4 pairs of axoneme Trophozoites in urine, urethral and vaginal secretions: siderophil granules

Amastigotes

Man

Intermediate Host (1o, 2o, etc) NONE

Man Mammals

Giardiasis; Traveller’s diarrhea Coating/carpeting of intestinal mucosa leading to fat malabsorption ● Abdominal pain ● Diarrhea ● Rotten egg-like flatus

Man

Trichomonas vaginitis; Pingpong infection ● Liquid green to yellow vaginal discharge ● Strawberry cervix ● Vaginitis ● urethritis ● Skin ulcer with elevated and indurated margin → ugly scar ● Painless ● No lymphadenopathy

Man

Sandfly (Phlebotomus spp.)

Leishmania braziliensis

● Espundia ● Tapir nose ● Chiclero ulcer (erosion of the pinna)

● Mucocuta neous or American Leishmaniasis Leishmania donovani

Trypanosoma cruzi

● Visceral Leishmaniasi ● Kala-azar ● Death fever ● Chagas

Clinical Presentation or Disease iulcer in colon Commensal

Metacyclic

Trypomastigote in

Man

Triatomine bugs

Visceral Leishmaniasis; Death fever; Reticuloendotheliosis Granulocytopenia and anemia ● Fever BID elevations ● Splenomegaly ● Cachexia ● Post kala-azar dermal leishmaniasis ● Chagoma

Prevention and Treatment Metronidazole

● Metronidaz ole 250 mg TID x 510 days ● Proper sanitary disposal of human feces

Oral metronidazole

● Meglumine antimonite ● Stiboglucon ate ● Pentamidin e ● Stiboglucon ate

● Pentamidin e ● Amphoterici nB

Page 8 of 33

● Nifurtimox

Scientific Name

Common Name Disease ● American Trypanosomiasis

Trypanosoma brucei gambiense Trypanosoma brucei rhodiense

Toxoplasma gondii

trypomastigote

Diagnostic Stage

Metacyclic Trypomastigote Trypomastigote in blood, CSF, LN aspirate

Toxoplasmosis

Mature oocyst Bradyzoites tachyzoites

Malignant tertian Subtertian

Malaria Plasmodium vivax

Benign tertian

Ovale malaria

Sporozoites

PARASITOLOGY Definitive Host

blood

Gambian West African Sleeping sickness Central Rhodesian East African Sleeping Sickness

Malaria Plasmodium falciparum

Malaria Plasmodium ovale

Infective Stage

Immature oocyst

Gametocyte and ring stage in blood - Vivax and ovale – Schuffner dots - Malari ae – bandshaped - Falcip arum – sausageshaped RBC: -

Vivax

Man

Cat

Man

Intermediate Host (1o, 2o, etc) (Triatoma, Rhodnius, Panstrongylus)

Tsetse fly (Glossina spp.)

Rodents Pigs Man

Anopheles

Clinical Presentation or Disease ● Fever ● Generalized lymphadenopathy ● Romana’s sign (eyelid and conjunctival edema) ● Chancre ● Headache ● Tachycardia ● Irregular fever ● Winterbottom’s sign (enlarged post. Cervical LN, non-tender) ● Kerandel’s sign (tremors, hyperesthesia) ● Encephalitis ● Myocarditis ● Focal pneumonia ● Retinochoroiditis ● Lymphoreticular hyperplasia ● Hepatosplenomeg aly ● Stillbirth ● abortion ● Chills ● Low grade fever ● Spiking fever at 40 C (except falciparum) ● Nephritic syndrome (Quartan nephrosis) – P. malariae Falciparum - Cerebral malaria - Malarial hyperpyrexia - Algid malaria - Blackwater fever - Hepatomegaly

Prevention and Treatment ● Benznidazo le ● Insecticide spraying ● Vector control ● Pentamidin e ● Suramin ● Melarsoprol ● DFMO ● Eflornithine

● Pyrimetham ine ● Sulfadiazin e ● Food protection ● Avoid unpasteurized milk ● Thoroughly cooked mean and eggs ● Chloroquine (DOC) ● Primaquine – for exoerythrocytic forms ● Parenteral quinine dihydrochloride ● Quinine gluconate ● Mefloquine ● Halofantrine

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Scientific Name Malaria Plasmodium malariae

Common Name

Infective Stage

Quartan malaria

Diagnostic Stage

PARASITOLOGY Definitive Host

Intermediate Host (1o, 2o, etc)

– young - Malari a – old - Falcip arum - all

Clinical Presentation or Disease - Normocytic anemia

Prevention and Treatment

Intermittent fever Increased susceptibility: Duffy factor Decreased susceptibility: G6PD trait, PABA deficiency, Sickle cell anemia

Medically Important Arthropod Dermatophagoids farinae Ticks/mites

Larvae

Larvae

Human

Adult lice

Nymph or adult lice (scalp)

Human

Causes Allergy

Dermatophagois pteronyssinus Pediculus humanus capitis

Lice

None (direct life cycle)

Red papules, 3 to 4 mm in diameter

● Avoid infestation with organisms ● Preventive clothing Pyrethrin

Purpuric halo Sarcoptes scabei

Scientific name Bacteriology Corynebacteria

Scabies

Common name “Coryneforms” “diphtherioid bacteria” “Diptheria toxin”

Burrowed eggs

Burrowed eggs

Pathologic Factors Diphtheria toxin – inhibits protein synthesis in all cells

Human

MICROBIOLOGY Host’s Immune Response

Fragement A- inhibits polypeptide chain elongation by inactivating the elongation of factor EF-2

Resistance depends on the availability of specific neutralizing antitoxin in the bloodstream and tissues

Tox gene

Immunity is based on documented childhood

Fomites

Diagnostics Diagnosis is usually clinical. Laboratory tests serve to confirm the clinical impression and are of epidemiologic significance. Dacron swabs – swabs should be collected from beneath any visible

Intense itching (may lead to secondary infection) Burrows and papules where mites are located. Generalized rash may occur in other areas Crusted, excoriated pruritic papules on the penis or buttocks is pathognomonic

Clinical presentation or disease Respiratory – pseudomembrane formation. Forceful removal will result into bleeding. Membrane coughed up after 5-10 days

● Permethrin 5% ● Lindane

Prevention/Treatment

Active immunization with diphtheria toxoid yields adequate antitoxin until adulthood – combined with tetanus toxoid and pertussis vaccine (DPT, DTaP, Td) “Bullneck” appearance – Children – primary caused by the enlargement immunization (3 doses); of the regional lymph nodes booster (2 doses) Page 10 of 33

Scientific name

Common name

Pathologic Factors Virulence is due to: - Capacity to establish infection - Rapid growth - Toxin Does not actively invade deep tissues

MICROBIOLOGY Host’s Immune Response immunizations and booster shots Antibody response to diphtheria toxin following clinical disease or to diptheria toxoid

Diagnostics membrane. Specimen must be obtained before antimicrobial drugs are administered Modified ELEK method – testing for toxin production PCR-based methods – testing for toxin production

Does not enter the blood stream

Clinical presentation or disease of the neck Myocardium – myocarditis Renal – Acute Tubular Necrosis

Prevention/Treatment Adults – primary immunization (3 doses); booster every 10 years Erythromycin and Penicillin

Peripheral nerve cells – delayed conduction

Supportive treatment – rest and airway management

Cutaneous diphtheria ELISA Schick test – intracutaneous skin test

Streptococci and Pneumococci

“strep throat”

Group A: - Capsule – composed of hyaluronic acid - M protein – antiphagocytic, anticomplementary - F protein – bacterial attachment - Lipoteichoic acid – mediated adherence to epithelial cells - Erythrogenic or pyogenic toxin - TSS toxin Group D: Extracellular dextran – helps to bind to heart valves Pneumococci: Pneumolysin – binds to cholesterol of host cell membranes

Capsular Hyaluronic Acid - when present inhibits phagocytosis Group Specific Polysaccharide Antigen Type Specific Antigen Toxins- Hemolysins, Pyrogenic exotoxin EnzymesStreptokinase, Deoxyribonucleases, Nicotinamide Adenine Dinucleotidase, Hyaluronidase

Group A: Inhibited by bacitracin PYR positive Dick test – used to confirm scarlet fever C-carb – used for lancefield groupings Group B: Gram stain Culture of urine, CSF, or blood Hippurate hydrolysis test (positive) CAMP reaction (positive)

Group D: Gram stain Culture (non-enterococci can only grow in bile; enterococci grow in 40% bile and 6.5% NaCl) S. viridians: Resistant to optochin S. pneumoniae:

Group A Pharyngitis

Penicillin G (DOC) Penicillin V

Scarlet fever Ampcillin Toxic shock syndrome Erythromycin Acute post-streptococcal glomerulonephritis Rheumatic fever – may follow streptococcal pharyngitis

ceftriaxone

Group B: Neonatal meningitis Neonatal pneumonia Neonatal sepsis

Group D: Subacute bacterial endocarditis Biliary tract infections UTI S. viridians: Subacute bacterial endocarditis Dental caries (by S. mutans) Brain or liver abscess Page 11 of 33

Scientific name

Common name

Pathologic Factors

MICROBIOLOGY Host’s Immune Response

Diagnostics Quelling test (positive) Does not grow in the presence of optochin and bile Dick Test- once commonly used to confirm Scarlet fever

Staphylococci

“Staph” “MRSA” for the methicillinresistant S. aureus

S. aureus: Capsule – inhibits chemotaxis and phagocytosis; facilitates adherence Protein A – binds to the Fc portion of the IgG molecules Teichoic acid – mediates attachment to mucosal surfaces Clumping factor – binds fibrinogen resulting in the clumping of the whole staphylococci in the presence of plasma Coagulase – clots plasma Lipases – lipid hydrolyzing enzymes Hyaluronidases – spreading factor Exotoxin – superantigen Enterotoxin – vomiting and diarrhea TSST-1 – toxic shock syndrome toxin Exfoliatin – scalded skin syndrome

Phagocytosis is inhibited

C-Carbohydrate- used for Lancefield groupings Gram stain: reveals gram positive cocci in clusters Culture: Beta hemolytic Produces a golden yellow pigment for Staph aureus Catalase postitive Beta hemolytic S. aureus: Coagulase positive Mannitol fermentation positive Susceptible to novobiocin

Clinical presentation or disease

Prevention/Treatment

Pneumococci: Pneumonia Meningitis Sepsis Otitis media (children)

S. aureus: Superficial localized - folliculitis, furuncles, carbuncles, impetigo

S. aureus: Penicillinase-resistant drugs

Deep localized - osteomyelitis, pneumonia, bacteremia endocarditis, pyoarthritis,

Vancomycin (for MRSA)

Gastroenteritis (onset 2-6 hours) Scalded skin syndrome

Rifampin

1st gen cephalosporins

S. epidermidis: Vancomycin

S. saprophyticus: Penicillin

Toxic shock syndrome S. epidermidis: Coagulase negative Susceptible to novobiocin S. saprophyticus Coagulase negative Not susceptible to novobioci

S. epidermidis: Bloodstream infections, surface infections, meningitis S. saprophyticus: UTI

S. epidermidis: Polysaccharide capsules S. saprophyticus Selectively adheres to urothelial cells via specific oligosaccharide receptors

Neisseriae

“gonococci”

N. gonorrheae:

IgA and IgG on mucosal

Specimen collection for

N. gonorrheae:

Ceftriaxone Page 12 of 33

Scientific name

Common name “meningococci”

Pathologic Factors Fimbriae/pili – adherence Lipooligosaccharide – elicits inflammatory response Op a (protein II) – invasion; outer membrane protein Por (protein I) – prevent phagolysosome formation in neutrophils; reduce oxidative burst Rm p (protein III) – block bacterial antibodies Tbp 1 & 2 – outer membrane receptors for transferring Lbp – outer membrane receptor for lactoferrin Extracellular IgA1 proteases – cleaves the H chain N. meningitides Polysaccharide capsule – antiphagocytic, antigenic Por proteins Opa class Pili LPS

MICROBIOLOGY Host’s Immune Response surfaces

Diagnostics culture and smear Culture: Nonselective medium – chocolate agar (from normally sterile sites) Selective media: - modified Theyer-Martin - Martin-Lewis - NYC agar Oxidase positive – key for identifying neisseria N. meningitides: 5% SBA Chocolate agar Presumptive – oxidase positive, gram negative diplococci

Clinical presentation or disease Ocular gonococcal infections - ophthalmia neonatorum (neonates) - Keratoconjunctivitis (adults) Urethritis

Prevention/Treatment Cefixime Doxycycline PO twice daily for 7 days Erythromycin Cefoxitin

Genital infections - gonococcal urethritis – scanty, clear/cloudy, copious and purulent discharge - gonococcal cervicitis – vaginal discharge; most common form of uncomplicated gonorrhea in women Vulvovaginitis

Crede’s prophylaxis (1% silver nitrate to the eyes of the newborn) – to prevent ocular infection

Disseminated gononcoccal infections - dermatitis-arthritis syndrome - Fitz-Hugh-Curtis syndrome – perihepatitis - PID - ARDS Meningitis

Rifampin – for penicillinallergic patients

N. meningitides Penicillin Chloramphenicol or 3rd gen cephalosporins

Chemoprophylaxis of close contacts Pregnant womanerythromycin PO 4xday for 7 days

N. meningitides Meningococcal pneumonia Anogenital infections Meningococcemia – mildest form; resolve spontaneously Acute meningococcemia – more serious; +meningitis Fulminant meningococcemia – strains that cause disseminated infections Meningitis – most serious; 2nd leading cause of communityacquired meningitis Primary meningococcal conjunctivitis Page 13 of 33

Scientific name Enteric Bacilli

Common name “honeymoon cystitis” – E. coli “traveller’s diarrhea” – ETEC “Freidlander’s bacillus” – K. pneumoniae “peptic ulcer” – H. pylori “rice-watery diarrhea” – V. cholera

Pathologic Factors E. coli: Common pili P pili Amfibrial adhesins Capsular polysaccharide Siderophores S fimbriae O antigens H antigens

MICROBIOLOGY Host’s Immune Response Specific antibodies develop in systemic infections

Diagnostics E. coli: Gram negative bacillus Indole positive Beta hemolytic Ferments lactose Culture – smooth, motile, flat, nonviscous colonies with distinct edges

K. pneumoniae: Polysaccharide capsule Endotoxin Enterotoxin

(+)sugar fermentation (+) TSI (-) citrate test K. pneumoniae: Gram negative coccobacillus Lactose fermenting Indole negative

Enterobacter: Cephalosporinases Vibrio: Cholera toxin

Culture – EMB or McConkey Enterobacter: (+) citrate (+) vogues-proskauer Campylobacter: Biology – G(-), spiral Culture – microaerophilic H. pylori: Tissue biopsy and culture Urea breath test Vibrio: Stool culture

Bacteroides &Fusobacterium

Gram- negative Bacilli

Bacteroides: B-lactamase Glycosidase enzymes Capsular polysaccharide Fusobacterium: Leukotoxin

Infection is usually enteric in nature T-cell dependent immune response

Foul smelling discharge; Infection in proximity to a mucosal surface; Gas in tissues Negative aerobic culture Bacteroides: Biological characteristics – obligate anaerobe, gram

Clinical presentation or disease E. coli: Diarrheal diseases - EPEC – pediatric diarrhea - ETEC – traveller’s diarrhea - EIEC – invasive diarrhea - EHEC – hemorrhagic colitis, hemolytic uremic syndrome UTI Neonatal meningitis

Prevention/Treatment E. coli: Treatment is usually based on symptoms K. pneumoniae: Aminoglycosides Third generation Cephalosporins Ciprofloxacin Enterobacter: B-lactamase inhibitors Carbapenems Aminoglycosides

K. pneumoniae: Epidemic diarrhea (newborns) UTI Lung abscess Septicemia Campylobacter: Fever, cramping abdominal pain, diarrhea, dysentery Gastroenteritis Guillain-Barre syndrome H. pylori: Peptic ulcer disease Predisposition to gastric carcinoma Vibrio: Watery stools with intestinal mucus and epithelial cells Violent vomiting Shock No fever Bacteroides: Peritoneal infections Bacteremia Peritonitis following rupture of viscus Subcutaneous abscess

Surgical drainage and antimicrobial therapy

Fusobacterium: Ulcerative colitis

Fusobacterium: Chloramphenicol

Bacteroides: Metronidazole Carbapenems

Page 14 of 33

Scientific name

Common name

Pathologic Factors

MICROBIOLOGY Host’s Immune Response

Diagnostics negative, rod-shaped Culture from blood, pleural fluid, peritoneal fluid, wounds, brain abscesses

Pseudomonas and other nonfermenting Bacilli

Pseudomonas Aeruginosa

Pseudomonas: Pili – adhesion Alginate (exopolysaccharide) – protects from phagocytosis in lung infections; produces septicemia in neutropenics Elastase

Pseudomonas: Sweet/grape-like/tacolike odor Usual sites of infection are the respiratory tract and burn lesions Recruitment of neutrophils

Pseudomonas: Grows well on most lab media: - TSI - McConkey agar - EMB agar - Mueller-Hinton agar

Clinical presentation or disease Periodontal diseases Lemierre’s syndrome Colon cancer

Pseudomonas: Most common sites of infection: - urinary tract - burns

Pseudomonas: Antipseudomonal penicillin + aminoglycoside Aseptic technique on hospital instruments and procedures

Subacute bacterial endocarditis

Nonlactose fermenter

Exoenzyme S – lung tissue destruction and bacterial dissemination

Oxidase positive

Swimmer’s ear – external otitis media

Beta hemolytic

Bacteremia and sepsis

Exotoxin A – causes tissue necrosis

Colony types: - fried egg appearance – large smooth, flat edges and elevated - mucoid appearance – alginate slime, usually from respiratory and urinary tract infections

Eye infections: - bacterial keratitis - neonatal ophthalmia

Shigella: Rectal swab or directly from ulcer

Shigella: Watery diarrhea (early stage)

Hemolysin – heat labile phospholipase C; heat stable glycolipid Pigments: - pyocyanin – “blue pus” - pyoverdin - pyorubin – red pigment - pyomelanin – black pigment Shigella: Large multi-gene virulence plasmid

Sereny’s test

Shiga toxin – similar to EHEC; enterotoxic, cytotoxic, neurotoxic

Salmonella: Blood/stool culture

Salmonella: Endotoxin Invasions

Typhidot test Widal test

Prevention/Treatment

Shigella: Ampicillin Amoxicillin Trimethoprimsulfamethoxazole Sanitational and personal hygiene Salmonella: Chloramphenicol

Chronic contiguous osteomyelitis

Ampicillin TMP-SMX

UTI

Quinolones

Malabsorption

Surgical removal of gall bladder

Fever and abdominal cramps

Vaccine (attenuated strain)

Lysine negative, nonmotile Severe keratoconjunctivitis and ulceration Salmonella: Enteric fevers Enteritis Enterocolitis Page 15 of 33

Scientific name

Common name

Pathologic Factors

MICROBIOLOGY Host’s Immune Response

Diagnostics

Flagella Vi antigen Resistance to acidic pH Hemophilus

Hemophilus Influenza

Capsular polysaccharide - typable – has 7 serovars - nontypable – lacks specific polysaccharides Somatic antigens - lipooligosaccharide - outer membrane proteins IgA protease

Clinical presentation or disease

Prevention/Treatment

Bacteremia/septicemia with focal lesions Inhalation of bacteria → colonization in the nasopharynx → penetration of the epithelium → invasion of capillaries Infants younger than 3 months may have serum antibodies transmitted from their mothers By age 3-5 years , many unimmunized children have naturally acquired anti-PRP antibodies that promote complement-dependent bactericidal killing and phagocytosis

Positive Quellung test Chocolate agar incubated aerobically at 10% CO2 Gram stain specimen - CSF - middle ear aspirates - thoracentesis - arthrocentesis ELISA Counter immunoelectrophoresis

H. influenzae: Encapsulated: - bacteremia - acute bacterial meningitis - cellulitis - osteomyelitis - joint infection - pneumonia Nontypable: - otitis media - sinusitis - pneumonia

Purified type b capsular polysaccharide vaccine Hib PRP vaccine Rifampicin Sulfonamides Chloramphenicol Trimetophrim Cefotaxime

H. parainfluenza: Usually after dental procedures Endocarditis H. aegyptus Pink eye – communicable purulent conjunctivitis Brazilian purple fever H. ducreyi Buboes – suppurative inguinal lymph nodes Chancroid – sexually transmitted painful genital ulcers

Aerobic Spore-forming Bacilli

“cutaneous anthrax” “inhalation anthrax” “gastrointestinal anthrax” – Bacillus anthracis

B. anthracis: -Protective antigen (PA) -Edema Factor (EF), -Lethal Factor (LF). PA binds to specific cell receptors, after proteolytic activation, membrane channel is formed that mediates entry of EF and LF to cell. EF is adenylate

B. anthracis: Spores germinate in the tissue at the site of entry. Growth of the organisms result in formation of a gelatinous edema and congestion. Bacilli spread via lymphatics to bloodstream, where

B. anthracis: Immunofluorescence staining techniques, PCR, ELISA Specimen: Fluid or pus from local lesion, blood, pleural fluid, and CSF in inhalational anthrax, stool or other intestinal contents in gastrointestinal anthrax

B. anthracis: Cutaneous anthrax: -Pruritic papule develops 1-7 days after spore entry. -black eschar lesion. -Marked edema -Lymphangitis and lymphadenopathy. -After 7-10 days eschar is fully developed. It dries,

B. anthracis: Tx must be started early. Ciprofloxacin is recommended for treatment. Penicillin G, Gentamicin, or Streptomycin were previously used. Prophylaxis with ciprofloxacin or doxycycline should be

Page 16 of 33

Scientific name

Common name

Pathologic Factors cyclase; with PA, it forms edema toxin. LF plus PA is lethal toxin, a major virulence factor and cause of death to those who are infected. Organisms proliferate at the site of entry. The capsules remain intact, the organisms are surrounded by proteinaceous fluid w/ few leukocytes from which they rapidly disseminate. B. cereus: Toxins that cause disease that is more of an intoxication than a foodborne infection.

MICROBIOLOGY Host’s Immune Response they multiply shortly before and after host’s death. In woolsorters’ disease, the inhaled spores are phagocytosed in the lungs, transported through lymphatics to the mediastinal lymph nodes, where germination occurs. B. cereus: Spores germinate, vegetative cells produce toxins during log-phase growth or during sporulation.

Diagnostics B. cereus: -presence of bacteria in patient’s stool is not sufficient to make a diagnosis because it may be present in normal specimens

Clinical presentation or disease loosens, and separates. Inhalation anthrax: -Incubation period- 6 weeks. -Marked hemorrhagic necrosis -Edema of the mediastinum. -Substernal pain and pronounced mediastinal widening visible on CXR. -Hemorrhagic pleural effusions follow.

Prevention/Treatment continued for 4 weeks while 3 doses of vaccines are being given for 8 weeks. B. cereus: Resistant to Penicillin and Cephalosporins. Serious non-foodborne infections should be treated with vancomycin or clindamycin.

Gastrointestinal anthrax: Rare in humans. -Abdominal pain -vomiting -bloody diarrhea Food poisoning: Emetic form: -1 to 5 hrs after ingestion of rice -nausea -vomiting -abdominal cramps -occasional diarrhea Diarrheal form: -1-24 hrs after ingestion of meat/sauce dishes -profuse diarrhea -abdominal pain and cramps B. cereus: Eye infections introduced through trauma/ foreign bodies: -severe keratitis -endophthalmitis -panophthalmitis Localized/ systemic infections: -endocarditis -meningitis -osteomyelitis Page 17 of 33

Scientific name Anaerobic sporeforming bacilli

Common name “botulism” – C. botulinum

Pathologic Factors C. botulinum: During autolysis of bacteria, toxin is liberated. Antigenic varieties: Types A, B, E, F (humans) Types A and B -variety of foods Type E -fish products C. tetani: Flagellar antigens C. perfringens Alpha toxin of C perfringens type A: lethicinase -splits lecithin to phosphorylcholine and diglyceride. DNase and hyaluronidase, a collagenase that digests SQ tissue and muscle are also produced. C. difficile -Pseudomembranes, microabscesses -C. difficile toxins

MICROBIOLOGY Host’s Immune Response C. botulinum: Botulinum toxin is absorbed from the gut and binds to receptor of presynaptic membranes of motor neurons of the peripheral nervous system and cranial nerves. Proteolysis inhibits the release of Ach at the synapse, resulting in lack of contraction and paralysis. C. tetani: Toxin binds to receptors on presynaptic membranes of motor neurons. Migrates by retrograde axonal transport to cell bodies of neurons to SC and brainstem. Toxin diffuses to terminals of inhibitory cells, including glycinergic interneurons and GABA-secreting neurons from brainstem. Release of glycine and GABA is blocked, motor neurons not inhibited.

Diagnostics C. botulinum: ELISA, PCR Specimen: -serum -gastric secretions -stool -leftover food C. tetani: Anerobic culture Primary differential dx: strychnine poisoning. C. perfringens Hemolysis and colony morphology, lecithinase activity, toxin production, neutralization C. difficile -Detection of one or both C. difficile toxins in stool -endoscopy

Clinical presentation or disease -pneumonia C. botulinum: -18-24 hours after ingestion -visual disturbances -inability to swallow -speech difficulty -signs of bulbar paralysis are progressi C. tetani: -Incubation period: 4-5 days -tonic contraction of voluntary muscles -pain may be intense -death may result from interference with the mechanics of respiration C. perfringens -Infection spreads in 1-3 days -crepitation in the SQ tissue and muscle -foul smelling discharge -rapidly progressing necrosis -fever -hemolysis -toxemia -shock

Prevention/Treatment C. botulinum: Canned foods/ preserved: -sufficiently heated to ensure destruction of spores -or boiled for 20mins before consumption Toxoids are used for active immunization in Africa. C. tetani: Prevention: -active immunization w/ toxoids -proper care of wounds contaminated with soil -prophylactic use of antitoxin -administration of penicillin C. perfringens: -early surgery (amputation) -antibiotic administration C.difficile: -Metronidazole -Vancomycin -Ampicillin -Clindamycin -Fluoroquinolones

C. difficile -Watery or bloody diarrhea -abdominal cramps -leukocytosis -fever

C. perfringens: The spores germinate at low oxidationreduction potential. Vegetative cells multiply, ferment carbohydrates present in tissue, and produce gas. Distention of tissue, interference with Page 18 of 33

Scientific name

Mycobacteria

Common name

“acid –fast bacilli” “tuberculosis” – M. tuberculosis “leprosy” – M. leprae “MAI” – M. aviumintercellulare “MAC”- M. avium complex

Pathologic Factors

M. tuberculosis: production and development of lesions -number of mycobacteria in the inoculum -type of host 2 principal lesions: -exudative type -productive type M. avium complex: ubiquitous M. leprae: unique odiphenoloxidase

MICROBIOLOGY Host’s Immune Response blood supply, secretion of necrotizing toxin and hyaluronidase favor the spread of infection. C. difficile: Cytotoxic activity: -binds to the brush border membranes of the gut at receptor sites. M. tuberculosis: When inhaled, organisms are deposited in alveoli. Immune system responds by release of cytokines and lymphokines that stimulate monocytes and macrophages. Mycobacteria begin to multiply within macrophages. 1-2 mos. after exposure, pathogenic lesions appear in lungs.

Diagnostics

M. tuberculosis: tuberculin test, sputum culture, PCR, M. avium complex: culture MAC organisms from blood or tissue. M. leprae: Specimen is smeared on slide and stained by the Ziehl-Neelsen technique

M. leprae: -Leprosy -Onset: insidious -Neurologic disturbances: anesthesia, neuritis, paresthesia, trophic ulcers, bone resorption, shortening of digits.

M. leprae: Cell mediated immunity is markedly deficient, skin is infiltrated with suppressor T cells

“Actinomycetoma” “Mycetoma” “Madura foot”

Nocardia: Neutrophilic inflammation (abscess formation),

Nocardia: impairs cell mediated immune response.

M. tuberculosis: -Pulmonary Tuberculosis -clinical manifestations are protean: -fatigue -weight loss -fever -night sweats -chronic cough -spitting of blood M. avium complex: Organ dysfunction: -pericarditis -soft tissue abscesses -skin lesions -lymph node involvement -bone infection -CNS lesions

M. avium complex: Opportunistic infection. CD4-positive lymphocyte count declines to below 100 microliters.

Actinomycetes

Clinical presentation or disease

Nocardia: Grows on most laboratory media, serologic tests not useful, molecular methods

Nocardia: Opportinistic infection. Begins as chronic lobar pneumonia

Prevention/Treatment

M. tuberculosis: 1st line drugs Rifampicin Isoniazid Pyrazinamide Ethambutol Streptomycin 2nd line drugs Kanamycin Capreomycin Ethionamide Cycloserine Ofloxacin Ciprofloxacin M. avium complex: -clarithromycin/ azithromycin + EMB -rifabutin -clofazimine Fluoroquinolones -amikacin M. leprae -Dapsone -RMP -clofazimine -minocycline -clarithromycin Nocardia: trimethoprim – sulfamethoxazole -amikacin

Page 19 of 33

Scientific name

Common name

Pathologic Factors Sulfur granules

MICROBIOLOGY Host’s Immune Response Pyogranulomatous reaction

Diagnostics required for specie-level identification. Sun ray appearance via gram stain of granules obtained from pus

Clinical presentation or disease -fever -weight loss -chest pain -spread from the lung often involves CNS, where brain abscess develops Mycetoma: -Madura foot -painless -begins at SQ tissue and spreads to adjacent tissues..

Spirochetes

“yaws” – T. pallidum subspecies pertenue “bejel” “endemic syphilis” – T. pallidum subspecies endemicum “pinta”- T. carateum “Lyme Disease” – Borrelia burgdorferri

T. pallidum: -Hyaluronidase: enhances invasiveness -Cardiolipin Borreliae: -antigenic structure variation B. burgdorferri: -bite of a small Ixodes tick -Large number of sequences for lipoproteins including outer surface proteins OspA to F.

Rickettsias

“Brill-Zinsser disease” – Rickettsia prowazekii “Rocky Mountain spotted fever” – Rickettsia rickettsii “Fievre boutonneuse” – Rickettsia conorii “Rickettsial pox” –Rickettsia

Rickettsiae: -peptidoglycan-containing muramic acid and diaminopimelic acid -lipopolysaccharide

T. pallidum: -Can penetrate intact mucous membranes. -Spread to nearby lymph nodes and then reach blood stream Borreliae: -Antibodies appear during febrile state, attack is probably terminated by their agglutinating ang lytic effects. B. burgdorferri: -after injection by the tick, organism maigrates out of the site, producing characteristic skin lesion -dissemination by lymphatics or blood to other sites Rickettsiae: -multiplies in endothelial cells of small blood vessels -produce vasculitis (lymphocytes surround blood vessels)

T. pallidum: -Dark-field examination -Immunofluoresence -Nucleic acid amplification tests Borreliae: -thin or thick blood smears stained with Wright or Giemsa stain -serology -animal inoculation B. burgdorferri: immunohistochemical methods -PCR -EIA or IFA + immunoblot assay Indian ink Silver impregnation methods Regain detection via non specific serological tests (Wassermen, Kahn, VDRL) Rickettsiae: -skin biopsies, -indirect immunofluorescence -enzyme immunoassays - Serology -PCR

T. pallidum: - papule develops at site of infection after 2-10 weeks -ulcer with clean, hard base (hard chancre) -“secondary” lesions appear: red macupapular rash. -syphilitic meningitis -chorioretinitis -hepatitis -nephritis -periostitis

Prevention/Treatment -imipinem -minocycline -linezolid -cefotaxime Mycetoma: -streptomycin -trimethoprim – sulfamethoxazole -dapsone Surgical debridement, penicillin T. pallidum: -Penicillin Borreliae: -Tetracycline -Erythromycin -Penicillin B. burgdoferri: - Doxicycline -Amoxicillin -Cefuoxime

Borreliae: -incubation period: 3-10days -sudden onset -fever and chills -during febril stages, organisms are present in the blood.

Rickettsiae: -fever -headache -malaise -prostration -skin rash (no eschar) -enlargement of spleen and

Rickettsiae: -Tetracyclines -chloramphenicol -florquinolones

Page 20 of 33

Scientific name

Common name

Pathologic Factors

akari “Queensland tick typhus”Rickettsia australis

MICROBIOLOGY Host’s Immune Response -cells become swollen and necrotic

Diagnostics

“Trachoma” – C. trachomatis “psittacosis” – human C. psittaci disease acquired from contact with birds

C. trachomatis: -Heparin sulfate-like proteoglycans C. pneumoniae: -glycan negative inclusions -sulfonamide resistant C. psittaci: -heat-stable -resists proteolytic enzymes -Lipopolysaccharide

C. trachomatis: - acute inflammatory changes in conjunctiva, scarring, eyelid deformities C. pneumoniae: - no signs and symptoms that specifically differentiate from those caused by other agents C. psittaci: -enters through respiratory tract -causes patchy inflammation of lungs, consolidated areas are sharply demarcated -exudates are predominantly mononuclear.

Prevention/Treatment

R. prowazekii: -lasts for about 2 weeks -more fatal in patients older than 40 y/o

Lymphocytic infiltrates in tissues. Polymorphonuclear leukocytes, macrophages, and lymphocytes are associated with blood vessels in the gray matter.

Chlamydia

Clinical presentation or disease liver

R. rickettsia: -rash appears in extremities first, moves centripetally

C. trachomatis - specimen stained with fluorescent antibody or by the Giemsa method -inoculation of specimen into cyclohex-imide-treated McCoy cell cultures -Immunofluorescence -PCR .C. pneumonia: microimmunofluorescence test C. psittaci: -PCR -DFA staining -immunoassay -complement-fixing or microimmunofluorescent antibodies in serum

R. akari: -rash that resembles varicella -firm red papule appears at bite site -develops into a deep seated vesicle -forms black eschar C. trachomatis: -incubation period: 3-10 days -lacrimation -mucopurulent discharge -conjuctival hyperemia -follicular hypertrophy -SEROVARS D-K: cause sexually transmitted diseases Men: -nongonococcal urethritis -epididymitis Women: -urethritis -cervicitis -PID

C. trachomatis -azithromycin -treatment must be simultaneous for both sex partners C. pneumonia: -macrolides -tetracycline C. psittaci: - treated based only on clinical diagnosis - doxycycline, erthromycin

C. pneumonia: -upper and lower airway disease occurs -Pharyngitis -Sinusitis -Otitis media C. psittaci: -sudden onset of illness, incubation of 10 days in average Page 21 of 33

Scientific name

Mycoplasma

Common name

“atypical pneumonia” – M. pneumoniae

Pathologic Factors

M. pneumoniae: -attachment to organism by a specific adhesion protein on the differentiated terminal structure of the organism - no cell wall, pleomorphic, can appear oblong shaped, motile Ureaplasma urealyticum: -requires 10% urea for growth -no cell wall, pleomorphic,

MICROBIOLOGY Host’s Immune Response

M. pneumoniae: -clinical spectrum ranges from asymptomatic infection to serious pneumonitis, with occasional neurologic and hematologic involvement.

Diagnostics

M. pneumonia: - clinical recognition of the syndrome -PCR -EIA M. genitalium: -NAATs -serology

Clinical presentation or disease -malaise -fever -anorexia -sore throat -photophobia -severe headache M. pneumonia: -incubation period: 1-3 weeks -insidious onset -malaise -headache -fever -sore throat -cough (paroxysmal) -blood-streaked sputum -chest pain -tracheobronchitis “Walking pneumonia”- aka atypical pneumonia, fever with a dry non productive hacking cough

Prevention/Treatment

M. pneumonia: can produce clinical improvement but do not eradicate: -tetracyclines -macrolides -fluoroquinolones

M. hominis: -salpingitis -tubo-ovarian abscesses U. urealyticum: -nongonococcal, nonurethritis in men -lung disease in premature low-birth weight infants M. genitalium: -acute/chronic nongonoccocal urethritis in men -cervicitis, endometritis, salpingitis, infertility in women. Virology The DNA viruses I Adenovirus

Adenoviruses

Toxic activity associated with pentons

Replication in nucleus of epithelial cells

Viral isolation from the eyes, throat, or urine; ELISA on fecal specimens on patients with GI infection

Localized infecion of eye, respiratory tract, GI tract, and urinary bladder

Contact and droplet precautions, and promptly respond to and report clusters of cases.

subclinical infections and can Page 22 of 33

Scientific name

Poxvirus

Common name

Vaccina, variola, mollluscum contagiosum, cowpox virus, paravaccinia virus, orf virus

Pathologic Factors

Produce eosinophilic inclusion bodies called Guarnieri bodies

MICROBIOLOGY Host’s Immune Response Replication in the cytoplasm of the cell

Diagnostics

Inoculation of embryonated eggs (traditional); Genome sequencing or microarray assays

DNA Virus II Herpes virus

Herpes Simplex Virus type 1 and 2

Ability to establish life-long persistent infections;

Varicella-Zoster virus (shingles)

ability to undergo periodic reactivation

HSV1: Upper and lower respiratory tract; HSV2: Genital route Varicella-zoster virus: cell mediated immunity

Cytomegalovirus Cytomegalovirus: evades immune elimination by protective coating of irrelevant host immunoglobulins

Epstein-Barr virus Herpes viruses 6 and 7

Epstein-Barr: EBVinfected B cells synthesize immunoglobulin; autoantibodies typical of disease

RNA Virus I Picornavirus

Enterovirus: Poliovirus, coxsackie virus A & B, Echovirus, Hepatitis A Rhinovirus: Common Cold Hepatovirus Parechovirus Aphthovirus: Foot and Mouth Disease Cardiovirus: Encephalomyocarditis virus, Theilovirus

viral replication in the tonsils, in the lymph nodes of the neck, Peyer’s patches, and the small intestine, then invasion of the Central Nervous System by way of circulating blood, Inflammation occurs secondary to the attack on nerve cells

Antibody and T cell production

HSV: Cytopathology; Isolation and identification of virus; Polymerase chain reaction Varicella-zoster: Tzanck smear; Immunofluorescence staining; electron microscopy; cell cutures; fluorescent antibody Cytomegalovirus: polymerase chain reaction and antigen detection assays; isolation of virus; serology

Clinical presentation or disease cause latent infections of lymphoid tissue Variola - smallpox

Prevention/Treatment

Vaccinia - mild disease

Vaccine: avirulent pox virus to induce immunity to virulent pox virus;

Molluscum contagioum virus - causes sexually transmitted disease mimicking genital herpes

Contact and droplet precautions, and promptly respond to and report clusters of cases.

HSV: necrosis of infected cells with inflammatory response

HSV: Acyclovir, valacyclovir, vidarabine

Varicella-zoster: generalized vesicular eruption of skin and mucus Cytomegalovirus: systemic infection in normal hosts; pneumonia in immunocompromised hosts Epstein-Barr:infectious mononucleosis

Varicella-zoster: Live attenuated vaccine, avoid direct contact; acyclovir, valacyclovir, famcyclovir, foscarnet Cytomegalovirus: Gangciclovir, foscarnet, acyclovir and valacyclovir Epstein-Barr: Acyclovir, adoptive transfer of EBVreactive T cells for EBV related lymphoproliferative disease

Epstein-Barr: Isolation and identification of virus; serology

Virus isolation, serology, PCR

Polio: fever, maaise Polio: Vaccination (IPV, OPV) headache, n/v, aseptic Salk-Killed vaccine: By meningitis (mild disease plus passes GI, only forms IgG Ab stiffness in back and neck), Sabin-Live attenuated flaccid paralysis vaccine, both IgG and IgA Coxsackie A: Herpangina Other enterovirus: proper (vesicular pharyngitis), hand hygiene foot and mouth disease, Coxscakie: no vaccines or acute hemorrhagic antiviral drugs available conjunctivitis, aseptic Rhinovirus: symptomatic meningitis Aphthovirus: formalinCoxsackie B: Pleurodynia treated vaccine [devil’s grip/Bornholm’s Hepatitis A: Inactivated Page 23 of 33

Scientific name

Paramyxovirus

Orthomyxovrus

Common name

Paramyxovirus: Parainfluenza 1-4, mumps, Newcastle disease virus, simian virus 5 Morbilivirus: Measles (rubeola), canine distemper virus Pneumovirus: Respiratory Syncytial Virus (RSV) Metapneumovirus: Human metapneumovirus Respirovirus: No common name Rubulavirus: No common name Henipavirus: Hendra virus, Nipah virus, Cedar virus Influenza A, B, C Thogotovirus H1N1

Pathologic Factors

MICROBIOLOGY Host’s Immune Response

Diagnostics

Virus replication is limited to the respiratory epithelium; involving nose and throat (most common), larynx and upper trachea; production of virus-specific IgE antibodies during primary infections; release of mediators of inflammation which alter airway function

Rubeola: interaction of T cells with virus RSV: IgA

Rubeola: History, multinucleated giant cells (Warthin-Finkeldy cells), lumbar tap Parainfluenza: nasal washings and respi secretions Mumps: history, gland enlargement, culture, multinucleated giant cell, serology

Hemaglutinin, glycoprotein on viral surface, binds to sialic acid on RBCs or cells of URT; and Neuraminidase, cleaves sialic acid to release newly formed virions from host cell

IgA, serum IgG, and cellular immunity

Cell culture in PMK or MDCK, hemadsorption to infected cells, Ab inhibition of hemadsorption, HSF, ELISA, HI H1N1: nucleic acid

Clinical presentation or disease disease] (epidemic myalgia), myocarditis, pericarditis Parechovirus: GI and respiratory illness, meningoencephalitis, otitis media, neonatal disease Rhinovirus: LRTI, sneezing, nasal obstruction, nasal discharge, sore throat, headache, mild cough, malaise, chilly sensation, otitis media, sinusitis, bronchitis, pneumonia Aphthovirus: fever, salivation, vesiculation of the mucous membranes of the oropharynx and of the skin of the pams, soles, fingers, and toes Cardiovirus: CNS involvement without myocarditis, flaccid paralysis Rubeola: fever, respi infections, maculopapular rash, koplik’s spot (pathognomonic), cough, coryza, conjunctivitis Parainfluenza: Laryngotracheobronchitis/croup, bronchiolitis, pneumonia, common cold in subclinical form Mumps: acute inflammation of the parotid glands, orchitis RSV: common colds, pneumonia, bronchiolitis, respiratory failure, otitis media, rhinitis, pharyngitis Influenza A: fever, malaise, headache, myalgia, anorexia, sore throat, dry cough, otitis media, myositis, croup, GI symptoms Influenza B: milder 3-day febrile with systemic

Prevention/Treatment vaccine

Rubeola: supportive, vitamin A, do not give aspirin Parainfluenza: supportive treatment, Ribavirin shows activity Mumps: supportive, live attenuated vaccine RSV: Ribavirin (inhalation), standard precaution, no vaccine

Amantadine hydrochloride, Rimantadine, Zanamivir, Oseltamivir H1N1: Oseltamivir (Tamiflu), Zanamivir (inhalation)

Page 24 of 33

Scientific name

Common name

Pathologic Factors

MICROBIOLOGY Host’s Immune Response

Diagnostics amplification test, Rapid influenza diagnostic test

Clinical presentation or disease symptoms, gastric flu Influenza C: afebrile URTI, confined to young children H1N1: fever, cough, sore throat, runny nose, body aches, headaches, chills, fatigue, vomiting, and diarrhea

RNA Virus II Coronavirus

Coronavirus: Severe Acute Respiratory Syndrome (SARS) Torovirus: enteric

Reovirus

Orthoreovirus, Rotavirus, Coltivirus, Orbivirus

Vaccines: Live attenuated nasal spray Killed injectable (IM): Trivalent (2 A strains + 1 B strain) or quadrivalent (2 A strains + 2 B strains)

Some viruses contain a third glycoprotein (hemagglutinin esterase); infections in humans usually remain in the upper respiratory tract

Resistance to reinfection may last several years but reinfections with similar strains are common.

Virus isolation (human embryo kidney, diploid cell lines), direct antigen detection, nucleic acid detection, serodiagnosis

Presence of spikes that form a “corona” around the virion.

Immunity is not absolute. Most patients (95%) developed antibody response to viral antigens detectable by flourescent antibody test or by ELISA.

Nucleic Acid and Antigen Detection by ELISA

Acute Gastro Enteritis

Viral isolation using primary Monkey Kidney Tissue culture, neutralization tests, ELISA

Low grade fever, rhinorrhea, pharyngitis, pneumonia, diarrhea, abdominal cramps, exanthema, aseptic meningitis, encephalitis

No treatment, wait for the clinical course to finish

Viral replication leads to increased intracellular Ca2+ level (effected by NSP4), increased Cl-

Rapid detection of rotavirus antigen in stool specimens Strains may be further characterized by enzyme

Rotaviruses Incubation period: 1-3 days Watery diarrhea, abdominal pain, vomiting

Supportive treatment

Replication takes place in cytoplasm Exhibits high frequency of mutation and recombination during each round of replication Pathogenic properties are primarily determined by the protein species found on the outer capsid of the virion

Specimen: Respiratory Secretions

Fever, coryza, cough, dizziness, (-) sore throat, chills/rigor, myalgia, headache, evidence of leucopenia, with absolute lymphopenia, rapid respiratory distress

Prevention/Treatment

No treatment and no vaccine. For the lower RTI: -3rd gen cephalosporin -oral clarithromycin -ribavirin -corticosteroid Isolate the patients, quarantine the exposed

Colds (afebrile), nasal discharge, malaise Incubation period: 2-5 days S/sx: 1 week duration

Stable at 50 C pH: 3-9 Replicates at cytoplasm Genetic reassortment occurs readily Wide range of hosts

Epidemic Acute Gastroenteritis Viruses

Rotaviruses -Groups A, B, C Enteric adenovius

(+) hemaglutinnin fir human O erythrocytes Outer capsid proteins VP4 and VP7 carry epitopes important in neutralizing activity, with VP7 glycoprotein being the

Rotavirus Vaccine (withdrawn due to intusussception

Page 25 of 33

Scientific name

Common name

Pathologic Factors predominant antigen.

Calicivirus -Norovirus -Sapovirus Astrovirus

Wide host range Infect cells of the villi of the instestine Multiply in their cytoplasm and damage their transport mechanisms

MICROBIOLOGY Host’s Immune Response secretion, and shut-off of host cell protein synthesis (effected by NSP3), resulting in acute osmotic and secretory diarrhea Nonspecific (innate) and acquired virus-specific humoral and cellular immune responses

Diagnostics immunoassay or reverse transcriptase polymerase chain reaction, but such testing is not commonly done. Immunoflourescence, ELISA, immune electron microscopy

Impaired sodium and glucose transportation

Clinical presentation or disease

Prevention/Treatment incidence)

-Group A: Single most important cause of endemic sever diarrheal illness in infants and young children worldwide -Group B: Diarrheal illness in adults and children in China -Group C: Sporadic cases and occasional outbreaks of diarrheal illness in children

Oral live attenuated pentavalent human- bovine reassortant rotavirus vaccine

Enteric adenovirus: Second most important viral agent of endemic diarrheal illness of infants of young children worldwide

Damaged cells slough off to the lumen and realease many viral particles

Calicivirus -Norovirus: Important cause of outbreaks of vomiting and diarrheal illness in older children and adults -Sapovirus: Sporadic cases and occasional outbreaks of diarrheal illness in infants, young children, and elderly adults Astrovirus: Sporadic cases and occasional outbreaks of diarrheal illness in infants, young children, and elderly adults

The RNA viruses III Rhabdovirus

Lyssavirus (Rabies)

Peplomers (spikes) composed of trimers of viral glycoprotein. G glycoprotein which is a major factor in neuroinvasiveness -bullet shaped -negative single stranded RNA -Non segmented - Helical, non capsid and is coiled into a bullet shape - replication in the cytoplasm

Has predilection for the hippocampus (Ammon’s horn cells)

Direct Flourescent antibody staining of biopsy or necropsy (standard diagnostics) RT-PCR, RFFIT, tissue staining to demonstrate Negri Bodies, corneal imprint, CT, MRI

Prodromal: -malasie, fatigue, headache, anorexia, n/v, restlessness, ill-defined anxiety, sore throat, fever, pain or paresthesia (close to the site of exposure)

No effective treatment

Encephalitic/ neurologic (Furious) type: -excessive restlessness,

Post exposure prophylaxis consisting of passive immunization with rabies

Milwaukee Protocol/ Wisconsin Protocol: chemically induced coma plus ribavirin and amantadine (still controversial)

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Scientific name

Togavirus

Common name

1. Alphavirus -ARBOvirus -Chikungunya -Mayaro virus -O’ Nyong Nyong virus -Ross River Virus -Semliki Forest Virus -Sindbis virus -Eastern Equine Encephalitis (EEE) -Venezualan Equine Encephalitis (VEE) -Western Equine Encephalitis (WEE) 2. Rubivirus -Rubella virus (German Measles)

Pathologic Factors

After subcutaneous inoculation, virus replication occurs in local tissues and regional lymph nodes. Then, virus enters the blood stream and is disseminated. Virus crosses the blood-brain barrier; widespread neuronal degeneration Alphavirus: Bite of a mosquito that has fed on animal viral reservoir Rubivirus: Fetuses infected during first 10 weeks of pregnancy

MICROBIOLOGY Host’s Immune Response

Antiviral antibodies appear in blood in 1-4 days of the onset of symptoms. Cell mediated immunity and interferon. IgG rubella antibodies persist for life.

Diagnostics

Clinical evidence and history, isolation and identification of virus during viremic phase. HI, ELISA, IF test, Nt test. Rise in IgG, presence of IgM.

Clinical presentation or disease uncontrollable excitement, agitation, confusion, hallucination, combativeness, seizures, opisthotonus, hydrophobia, foaming of mouth, aerophobia Paralytic (Dumb) type: -flaccid ascending symmetric paralysis, sensory abnormalities, decreased tendon reflex, coma, respiratory and circulatory collapse which lead to death -Syndromes range from benign febrile illness to severe systemic disease with hemorrhagic manifestations or major organ involvement -neurotrophic alphaviruses can produce severe destructive CNS disease with serious sequelae -Chikungunya, Ross River, and Mayaro: cause painful arthritis that persist for weeks after the initial febrile illness -Human illness disease patterns: Chikungunya virus: the prototype for those causing an acute febrile illness with malaise, rash, severe arthralgias, and sometimes arthritis. O’Nyong Nyong, Mayaro, and Ross River causes similar identical clinical manifestations -viremia coincident with abrupt onset of fever, chills, malaise, and joint aches. Subsides in 3-5 days.

Prevention/Treatment immunoglobulin and immunization with a vaccine

Treatment is supportive. Vaccine is available (MMR)

Rubella (German Measles) Page 27 of 33

Scientific name

Flavivirus

Common name

West Nile virus, dengue virus, yellow fever virus. St. Louie encephalitis virus, Hepatitis C virus

Pathologic Factors

Virus replication occurs in local tissues and regional lymph nodes after subcutaneous inoculation. Enters the blood stream and is disseminated. Crosses the blood-brain barrier; widespread neuronal degeneration

MICROBIOLOGY Host’s Immune Response

Inhibit/ evade innate and adaptive immune response Humoral and cell mediated immunity

Orthobunyavirus (California Encephalitis Virus)

Vector borne virus (mosquitos, ticks, sandflies)

West Nile: Serology of blood serum and CSF; detection ofvirus specific IgM an neutralizing antibodies Dengue: cell culture, PCR, viral antigen detection, serology

The virion RNA is infectious and serves as both the genome and the viral messenger RNA. The whole genome is translated in a polyprotein, which is processed co- and post-translationally by host and viral proteases.

Bunyavirus

Diagnostics

Yellow Fever: ELISA, iver biopsy

Replicate within the cytoplasm and bud from

HI, ELISA, Nt test, PCR

Clinical presentation or disease -lymphadenopathy, and maculopapular rash, swollen glands, arthralgia, arthritis, thrombocytopenia, postinfectious encephalitis. Morbilliform rash. Congenital Rubella Syndrome: Deafness, visual defects, cataract, corneal opacity, all severe and bilateral -TRIAD: eyes, ears, heart West Nile: West Nile Fever, West Nile Neuroinvasive disease (meningitis, encephalitis, meningoencephalitis, poliomyelitis-like syndrome), rashes Dengue: -Febrile phase: sudden-onset fever, headache, mouth and nose bleeding, muscle and joint pains, vomiting, rash, diarrhea - Critical phase: hypotension, pleural effusion, ascites, GI bleeding - Recovery: altered level of consciousness seizures, itching, slow HR Yellow Fever: fever, headache, chills, back pain, fatigue, loss of appetite, muscle pain, nausea, and vomiting. Liver damage (jaundice, abdominal pain). Bleeding in the mouth, the eyes, and the gastrointestinal tract will cause vomit containing blood Orthovirus: severe bifrontal headache, fever, vomiting,

Prevention/Treatment

West Nile: No specific treatment; supportive care (IV fuids, respiratory support) Dengue: symptomatic relief Yellow Fever: Hospitalization, intensive care for rapidly deteriorating cases

HRFS: Supportive treatment, rodent control.

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Scientific name

Common name Hantavirus (Hemorrhagic fever with Renal Syndrome [HRFS] and Hantavirus Pulmonary Syndrome [HPS]) Phlebovirus (Sandfly fever and Rift Valley Fever)

Arenavirus

Pathologic Factors Interact with viruses that are closely related serologically to produce recombinant viruses by genetic reassortment

MICROBIOLOGY Host’s Immune Response the membranes of Golgi apparatus

Diagnostics

Clinical presentation or disease lethargy, convulsions, seizures, aseptic meningitis HRFS: interstitial nephritis, generalized hemorrhage, shock, nephropathia epidemica HPS: prodromal fever, myalgia, cough, headache, rapidly progressive pulmonary edema, functional impairment of vascular endothelium Sandfly fever: mistaken for malaria, headache, malaise, nausea, fever, photophobia, stiffness of the neck and back, abdominal pain, and leucopenia Rift Valley Fever: mild febrile illness, retinitis, encephalitis, hemorrhagic fever Lassa Fever: fever, mouth ulcers, severe muscle aches, skin rash with hemorrhages, pneumonia, heart and kidney damage Lymphocytic Choriomeningitis: fever, chills, malaise, generalized muscle aches and pains, weakness, headache, and sore throat, hydrocephalus, blindness, fetal death.

Prevention/Treatment HPS: adequate oxygenation, Ribavirin Sandfly fever: all patients recover, no treatment needed Rift Valley Fever: mosquito control

-Lassa Fever -South American Hemorrhagic Fever -Junin Hemorrhagic Fever -Argentine Hemorrhagic Fever -Machupo Hemorrhagic Fever -Venezuelan Hemorrhagic Fever -Lymphocytic Choriomeningitis

Infectious through aerosols – great caution is needed in handling the specimens Both vertical and horizontal transmission possible No cytopathic effects

T-Cell mediated inflammatory response

ELISA, immunohistochemistry, reverse transcriptase polymerase chain reaction assays

Ptyriasis Versicolor (An-An)

Lipophilic yeast invading the stratum corneum

Inflammation (minimal response)

KOH stain or Calcofluor White

Ketoconazole shampoo (dandruff) Topical Imidazole

Seborrheic dermatitis and Dandruff Tinea nigra

Cosmetic fungal infection of skin and hair shaft Discrete, serpentine, hyper/hypopigmentd macules on skin

Infection of the stratum corneum

Can be asymptomatic

Light microscopy (10% KOH)

Dark discoloration often on the palms (brown to black)

Piedraia hortai

Black Piedra

Infection of the hair shaft

Minimal response

Light microscopy (10% KOH)

Trichosporon spp.

White Piedra

Superficial nodular infection of the hair Larger, softer yellowish

Keratolytics, salicylic acid and azole derivatives, benzoic acid compound Removal of the hair and topical antifungal

Mycology Malassezia globosa

Pityriasis foliculitis

Hortaea werneckii/ Exophiala werneckii

Lassa Fever: adequate oxygenation, Ribavirin. Vaccine is available for Junin Virus.

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Scientific name

CUTANEOUS Dermatophytosis Microsporum

Common name

Tinea/Ringworm

Trichophyton

Tinea Pedis – foot “athelete’s foot”

Epidermophyton

Tinea Manus - hand

Pathologic Factors

MICROBIOLOGY Host’s Immune Response

Diagnostics

Clinical presentation or disease nodules White Piedra: axilla or scalp; soft whitish granules Black Piedra: hard, black nodules of the scalp, facial hair and pubic hair

Prevention/Treatment

Utilization of Keratin as nutrient source. Keratinised stratum corneum is simply colonized.

Allergic and inflammatory eczematous response

Direct microscopy (10% KOH) of skin and scalp scrapings Culture: SDA

Tinea / Ringworm of the scalp, glaborous skin and nails.

Topical antigungal agent Systemic Therapy

Thermotoerance, adhesion, melanin production, ergosterol peroxide

Innate (complement system activation), Acquired immunity (activated macrophages), Humoral response driven by IL-2

KOH Mount

Nodular lesions in the skin at point of entry and along lymph nodes and vessels. May develop into chronic ulcer

Potassium Iodine (oral) Itraconazole Amphotericin B Newer Triazoles

Tinea Cruris – thighs and buttocks Tinea Unguium - nails (Dermatophyte onychomycosis) Tinea Corporis – skin on the body Tinea Capitis - scalp SUBCUTANEOUS Sporotrichosis Sporothrix schenkii

Gardener’s Disease/ Rose Gardener’s Disease

Pulmonary sporotrichosis

Chromoblastomycosis Phialophora verrucosa Fonsecaea pedrosai

Lobomycosis Loboa loboi

Direct Microscopy (10%KOH)

Lobo’s disease

Stimulates transforming growth factor β1 and IL-10 which

Granulomatous reaction

KOH Mount

Disseminated sporotrichosis (osteoarticular sporotrichosis, sporotrichosis meningitis) Infection of the cutaenoues and subcutaneous Dematiaceous, planatedividing, rounded sclerotic bodies Crusted, verrucose, wart-like lesion Chronic keloidal lesions. Painless, but may become

Surgical excisiojn Flucystosine

Sulfa drugs

Page 30 of 33

Scientific name

Common name

MICROBIOLOGY Host’s Immune Response

Pathologic Factors

Diagnostics

inhibitsthe cellular immune response and, as a consequence, the activation of macrophages Rhinoentomophthorom ycosis

Biopsy, Serology

Clinical presentation or disease veruccous an ulcerative

Hard nodules developing in the nasal area leading to a large disfiguring tissue mass

Prevention/Treatment

Surgery,

Entomophthora coronate

SYSTEMIC AND OPPORTUNISTIC Blastomyces dermatides

I Gilchrist’s disease

Thick cell wall; BAD-1

Phagocytosis and killing by neutrophils, monocytes, and alveolar macrophages

KOH mount, Culture, EIA, Imaging

South American bastomycosis

Cell wall

Granuomatous infitration

Culture, serology, direst microscopy

Coccidioides imitis

San Joaquin Valley fever

Spherules trigger acute inflammatory reaction and is resistant to eradication by host’s immune system

Direct microscopy

Histoplasma capsulatum

Histoplasmosis

Yeasts may produce proteins that inhibit the activity of lysosomal proteases.

Complement activation; T-cell and cytokines facilitate killing of the organism; Macrophages kills spores Fungistatic properties of neutrophils and macrophages. T lymphocytes are crucial in limiting the extent of infection.

Candida albicans

Candidiasis



Surface molecules that permit adherence of the organism to other

 



Intact mucocutaneous barriers

 Acid proteases and phospholipases that involve



Phagocytic cells

traconazole

Granulomatous lesions and abscess

Paracoccidiodes brasilensis

Inflammatory response produces calcified fibrinous granulomas with areas of caseous necrosis.

Pulmonary manifestations may mimic PTb

Serology, antigen testing

Wet mount, scrapings, smears, endoscopy, urinalysis (depending on the manifestation)

Crusty cutaneous esions Membrane ulceration and spread through the lymphatics Flu-like symptoms, erythema nodosum, well defined lung cavitation, dissemination into other organs, verrucous plaques Pneumonia, disseminated disease in immunocompromised persons, cavitary pulmonary lung disease, calcified lymph nodes, mediastinal fibrosis, erythema nodosum, erythema multiforme, and thrombocytopenia Chronic mucocutaneous candidiasis: disfiguring lesions of the face, scalp, hands, and nails. Chronic mucocutaneous candidiasis is occasionally associated with oral thrush and vitiligo.

Amphotericin B Itraconazole Amphotericin B

Itraconazole, amphothericin

Mucocutaneous: nystatin, clotrimazole, ticonazole, fuconazole, ketoconazole Systemic: amphotericin B, oral flucytosine, fluconazole, caspofungin

Page 31 of 33

Scientific name

Common name

MICROBIOLOGY Host’s Immune Response

Pathologic Factors

 

penetration and damage of cell  envelopes  Ability to convert to a  hyphal form (phenotypic  switching)

Diagnostics

Clinical presentation or disease Oropharyngeal candidiasis: Sore and painful mouth, burning mouth or tongue, dysphagia, thick, whitish patches on the oral mucosa, diffuse erythema and white patches that appear on the surfaces of the buccal mucosa, throat, tongue, and gums.

Polymorphon uclear leukocytes Monocytic cells

 

Complement

 

Immunoglob

Esophageal candidiasis: Dysphagia, odynophagia, retrosternal pain, epigastric pain, nausea and vomiting

ulins

 

Cellmediated

Nonesophageal gastrointestinal candidiasis: epigastric pain, nausea and vomiting, abdominal pain, fever and chills, abdominal mass (in some cases)

 

Cryptococcus neoformans

Cryptococcosis

Cryptococcal polysaccharide capsule has antiphagocytic properties and may be immunosuppressive. The antiphagocytic properties of the capsule block recognition of the yeast by phagocytes and inhibit leukocyte migration into the area of fungal replication.

Mucocutane ous protective bacterial flora Damage/ deficiency of the aforementioned increases the likelihood and severity of infection. Cell-mediated immunity

Prevention/Treatment

Genitourinary tract candidiasis

 Direct examination, culture,  histopathology, serology

Cough with the production of scant mucoid sputum, pleuritic chest pain, ow-grade fever, dyspnea, weight loss, and malaise

Amphotericin B, fluorocytosine, fluconazole

Meningitis and meningoencephalitis: Headache, confusion, lethargy, obtundation, coma, normal or mildly elevated temperature, nausea and vomiting (with increased intracranial pressure), fever and stiff neck (with an aggressive inflammatory response; less common), Page 32 of 33

Scientific name

Aspergillus sp.

Common name

Aspergillosis

Pathologic Factors

Macrophages and neutrophils encompass, engulf, and eradicate the fungus.

MICROBIOLOGY Host’s Immune Response

Toxic metabolites that inhibit macrophage and neutrophil phagocytosis.

Diagnostics

Clinical presentation or disease blurred vision, photophobia, and diplopia, hearing defects, seizures, ataxia, aphasia, and choreoathetoid movements

Direct examination, culture,  KOH mount (dependin on the manifestation)

Ranges from hypersensitivity reactions to direct angioinvasion:

Prevention/Treatment

Surgical removal Amphotericin B, itraconazole

 

Allergic bronchopulmonary aspergillosis (ABPA)

  

Chronic necrotizing Aspergillus pne umonia Aspergilloma

  Rhizopus, Mucor, Cunninghamella, Apophysomyces, Absidia, Saksenae and Rhizomucor sp.’s

Mucormycosis

Neutrophils are the key host defense against these fungi.

Direct examination, culture

Invasive aspergillosis Rhinocerebral mucormycosis: (thrombosis, necrosis, invasion of the sinuses,eyes, cranial bones and brain, BV and nerve damage, edema of the facial area, bloody nasal exudates and orbital cellulitis)

Surgical debridement Amphotericin B

Thoracic mucormycosis: (invasion of lung parenchyma and vasculature, causing ischemic necrosis and tissue destruction)

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