Shared Flashcard Set


Important facts about important bugs for test

Additional Biology Flashcards




Which Intestinal Nematodes arrive in the gut of humans through penetration of the skin by their larval forms?
1) Strongyloides stercoralis (Hyper-infections in HIV)

2) Hookworm

Treat with Ivermectin or Albendazole
Which Intestinal Nematodes arrive in the gut via ingestion of infective eggs?
1) Ascaris (Abdominal discomfort
2) Pinworm (Perianal itch)
3) Whipworm (Abdominal discomfort)

Treat with Ivermectin or Albendazole
What is the life cycle of Trematodes (flukes)?
Parasitic flatworms with genus "Shistosoma"

Acute (Katayama Fever)
Chronic (Bladder cancer, liver disease, Neuro)

1) Grab onto snails in fresh water and release Cercariae
2) Enter human skin and go to lungs/liver to Mature
3) Go to bladder and GI tract via Veins
4) Released in Urine/Feces

Treat with Prazinquantel
Which Tapeworm (Cestode) causes Neurocysticercosis?
Taenia solium (PIG!) causes seizures in Latin America and Asia
Which Tapeworm (Cestode) uses Dogs as a carrier, leading to liver cysts and sometimes shock?
Echinococcus goes in Dog's poop and can cause Hydatid Disease.

Eggs form Oncospheres in GI, which penetrate the mucosa, and enter circulation to get to the liver.
How do you treat the Ectoparasites?
Scabies (allergic reaction to fees)- Permethrin

Lice - Permethrin/Ivermectin

Myiasis- Maggots- NO SURGERY
What is the lifecycle of the parasite that causes liver abscesses and bloody diarrhea in Mexico?
Entamoeba histolytica (treat with Metranidazole)

1) Cysts in environment are ingested

2) Becomes trophozoite in gut, which penetrates colonic mucosa to get to portal circulation and the liver
What parasite is picked up from dirty contact lenses?
Which parasites cause prolonged, watery diarrhea and non-bloody, fowl-smelling explosive diarrhea, respectively?
Watery= Cryptosporidium (extracellular)

Explosive= Giardia (intracellular)
How might you treat an infection that manifests with vaginal discharge/fishy odor in women but is asymptomatic in men?
This sounds like Trichomonas vaginalis

What is the lifecycle of a parasite that infects RBCs particularly severely in cases of functional Asplenia in the Northeastern US?
Babesia (Maltezec cross in RBC)

1) Deer and white-footed mice are bitten by Ticks
2) Ixodes ticks bite humans
Which parasite is carried by the Sandfly in the middle east and africa?
Leishmania spp. cause visceral and ulceritic disease
What is the geographical location and vector of the pathogen that causes "Chagas Disease"?
Trypanosoma cruzi (South America) carried in "Kissing Bugs" causing GI dysmotility and heart Failure.
What is the geographical location and vector of the pathogen that causes "Sleeping Sickness"?
African Trypanosome carried in Tsetse Fly in Africa

Causes Sleeping Sickness and fatal Meningo-Encephalitis.
When might you see Toxoplasma, Microsporidia and P. jirovici infections?
HIV or other case of T-cell suppression.

1) Toxoplasma (retinitis or brain abscesses if reactivated)
2) Microsporidia (diarrhea)
3) P. jirovici (Pneumonia)
What is the pathogenesis of the fungi that produces Aflatoxin B and can cause Hepatocellular Carcinoma?
Aspergillus fumigatis Mold (treat with Voriconazole)

** Problem in immunocompromised **

1) Inhalation of spores
2) Evasion of pulm macrophages and PMNs
3) Local lung infection
4) Hematological spread
How do you treat a patient who presents with oral thrush, diaper rash and abscesses following GI surgery?
Sounds like Candida albicans yeast (normally in Vag, GI and mouth)

1) Treat topically with Nystatin and Imidazole

2) Treat systemically with Amphotericin B, Fluconazole or Echinocandin
How do you diagnose/treat the pathogen that has a resistant polysaccharide capsule, grows at normal human BP and produces melanin to resist oxidative stress?
Crytpococcus neoformans Yeast (Meningitis)-

**CD4+ usually directly inhibits**

1) Diagnose with india ink for capsule in CSF

2) Treat with Flucytosine-5 + Amphotericin B.
Which fungi that branches at right angles is most concerning for mortality by thrombolic embolism?

What is the life-cycle?
Zygomycoses (Mucor, Absidia, Rhizopus, Rhizomucor)

**Occur in immunocompromised states, metabolic disease or hemochromatosis**

1) Spores enter respiratory tract and deposit in nose or alveoli

2) Adhere to vascular structures (cause brain/nose infection)
What is the clinical manifestation of the fungi that is transmitted through plant thorns?
Sporotrichosis mold

1) Non-healing inflamed nodule

2) Lymphatic spread to cause red, nodular lesions
Where is the geographic location of the fungi that causes Mediastinal granuloma and fibrosis, but that is often unrecognized as a primary infection?
Histoplasma capsulatum (Dimorphic- yeast in host and mold in enviornment)

**Look in urine or tissue**

Found in Ohio and Mississippi River Valley
How would you treat the dismorphic fungus found primarily in the Southwest US?
Coccidiodes immitus causes "Valley Fever" with peripheral eosinophila and sometimes systemic spread

Treat with Amphotericin B
How do you treat the fungi that causes Pneumonia in HIV patients?
P. jirovici (lacks ergosterol)

Bactrim (TM/SFX)
How do you diagnose/treat the organisms that causes "Jock Itch" and "Athletes Foot"?
Trichophyton rubrum

1) Diagnose with skin scratch
2) Treat with Terbinafine (oral) or Imidazole (Topical)
What kind of infection presents as a polymicrobial, antibiotic-resistant abscess?
Non-clostridial Anaerobic infection (Bacteroides-like)
Which non-spore-forming, gram-negative anaerobes colonize the colon, vagina and mouth?
Bacteroides spp.

1) B. fragilis makes enterotoxin

2) Bile-sensitive species are Porphyromonas and Prevotella (endotoxic activity)

3) B. fragilis and P. melaninogenica make capsule
What is the life cycle of the gram-negative anaerobic bug that is normally found in the colon, and that can cause peritonitis and abscess formation?
Bacteroides fragilis causes endogenous infections by breeching the epithelium in surgery/wound/ruptures.
How do you treat the gram-positive organism that manifests with purple lesions, bloody stool and gas buildup?
Clostridia perfringens (C. septicum would be GI cancer) is treated with surgical removal and hyperbaric O2
What is the infectious life cycle of the organism that causes spastic paralysis by inhibiting glycine/GABA signaling?

How can you treat?
C. tetani implants spores at wound or during childbirth, where they germinate (if redox is low) into a new cell and make tetanis toxin.


Treat with antitoxin and prevent with Tetanus toxoid in DPT.
Which organisms are known to undergo genetic transformation?
All encapsulated, extracellular pathogens

1) Streptococcus

2) Haemophilus (between segmented genomes within host)

3) Neisseria (pili and OpA)
What virulence factors are carried on the pXO1 and pXO2 plasmids?
This is Bacillus antracis!

1) pXO1 is anthrax toxin
2) pXO2 is polypeptide capsule
What treatment(s) is available for the non-enveloped dsDNA viruses?
1) Papovaviruses (circular)- HPV vaccine, Imiquimod/IFN-a

2) Adenovires (linear)- None
What treatments are available for the enveloped dsDNA viruses?
1) Hepadnavirus (HBV)- Vaccine, Lamivudine/INF-a

2) Herpesvirus
HSV- Valacyclovir/Foscarnet
CMV- Gancyclovir/Cidofovir/Foscarnet
VZV- Vaccine, Valacyclovir
EBV- None
What treatment is available for a non-enveloped ssDNA virus that utilizes the host-cell DNA polymerase?
Parvovirus (AAV)- None known
Which DNA viruses are enveloped?
- Hepadna (circular)
- Papovavirus (circular)
- Adeno (linear)
- Iridovirus
What is the life cycle of the infection caused by the only DNA virus that replicates in the cytoplasm?
This is Poxvirus (complex, enveloped DNA virus)

1) Transmitted in aerosole with 10-14 day incubation followed by 5 days of rash (maculopapular, vesicle, postule, crust, scar)

2) Vaccine grown in vero cells that cannot be given in immune-compromise, eczema contradiction or pregnancy
What treatments are available for un-enveloped, ss-RNA (+) viruses?
These include Picornaviruses (Polio, HepA and Rhinovirus) and Caliciviruses (Norovirus and Hep E).

For HepA, can try killed-vaccine and HAV vaccine

Basically nothing- they are hard to treat without envelope!
What treatments are available for enveloped, ss-RNA (+) viruses?
1) Togavirus (rubella)- nothing

2) Coronavirus (SARS)

3) Flavivirus (WN, Dengue and HCV)- HCV (Ribavirin/IFN-a/Teleprevir or Boceprevir

4) Retrovirus (HIV)- ART (protease, integrase, capsid, ect)
What treatments are available for a virus that replicates in the nucleus?
The only RNA virus that make RNA and mRNA in nucleus is Influenza (segmented, ssRNA(-), enveloped virus)

For influenza A- Rimantadine/Amantadine and Oseltamivir/Zanamivir

For influenza B- only Oseltamivir/Zanamivir
How does Ebola virus replicate?
Ebola virus is a Filovirus, which is a ssRNA(-) virus, so it must carry its only RdRp.

1) In cytoplasm, RdRp makes +RNA (replicative complex)

2) RdRp makes more -RNA

3) Structural proteins from +RNA, package with -RNA and RdRp to generate virion progeny.
True or False:

HIV uses host machinery to transcribe viral mRNA

Usually, this occurs with viral RdRp, but in this case, mRNA transcription occurs after integration into the host genome, and therefore makes use of the use machinery.
What is the lifecyle of the virus that is treated with Lamivudine?

1) Gapped dsDNA repaired in nucleus

2) Viral mRNA and pregenomic RNA made using host cell machinery

3) Pre-genomic DNA goes to cytoplasm where it is template for RT within newly formed viral particles.
How do you treat viruses that cause Syncytia formation?
Syncitia is fusion of multinucleated giant cells and you see it in RSV and HSV

RSV- Palivizumab for viral entry ($$) or Ribavirin

HSV- (Val) acyclovir, Foscarnet
Which viruses can be diagnosed with a Plaque assay vs. Focus-forming assay?
1) HSV and AV (involving cell lysis)

2) HIV
What kinds of viruses (i.e. ss(-), ss(+), envelope, ect) exhibit latent infection/reactivation?
1) CMV EBV, HSV, VZV- Herpes (dsDNA-enveloped)
2) HIV- Retro (dsDNA-enveloped)
What is the pathogenesis of the virus that uses 2A protein to inhibit eIF46 and 2BC/3A to inhibit cell secretory pathways?
This is Polio virus (Pocornavirus- non-enveloped ssRNA(+)

1) Enters GI (fecal oral) (90% asymptomatic)

2) Hematologic spread to liver and spleen for secondary replication

3) some spread to CNS to cause meningitis/encephalitis

4) Small percentage of CNS infections lead to paralytic poliomyelitis (flacid)

** 2A (eiF4G), 2BC/3A (secretory path), 3C protease (Tbp for TFIId)
What is the viral life cycle to the pathogen that causes Paralytic poliomyelitis in a small percentage of hosts.
Polio virus (ssRNA(+), non-enveloped)

1) Binds Pvr receptor and undergoes endocytosis with conformational change (VP1 and VP4 for fusion)

2) Replicates in cytoplasm with assembly and eggression (90% asymptomatic)

VIRULENCE** 2A (eiF4G), 2BC/3A (secretory path), 3C protease (Tbp for TFIId)
What is Pleconaril used for?
Enteroviruses and Polio + other picornaviruses
How does HIV achieve early and late-phase protein translation?
1) After entering through CD4/CXCR4, Virion-associated RT makes circular dsDNA, which is integrated into the nucleus

2) TAT interacts with HIV LTR t omake RNAP11 (early)

3) REV binds cis sequences in RNA to initiate late gene expression.

4) Protease makes RT and IN from GAG-POL and SU (gp120) and TM (gp41) from ENV precursor protein.
How can you treat the virus that utilizes RT to make DNA from pre-genomic DNA?
Tenofovir, Emtricitabine, Lamivudine and Adefovir
What side effects are associated with the treatment a case of Herpes Encephalitis?

What about VZV?
Acyclovir Empirically at a high dose- Nephrotoxicity (CRYSTALS IN RENAL TUBULES)

For VZV (<3 days only), also use high dose Acyclovir
How might you go about treating herpes labialis?
Topical cream- Penciclovir (nucleoside analogue)

**Famciclovir is the pro-drug**
What side effects are associated with the treatment for gancyclovir-resistant CMV?
This is CIdofovir or Foscarnet

Cidofovir= **Nepthrotixicity, GI and Neutropenia

Foscarnet= **Nephrotoxicity and Electrolyte imbalance***
also penile ulcers are possible
What is the difference in side effects between the two drugs used to treat Influenza B?
Oseltamivir- Capsule causes vomiting

Zanamivir- Power that can cause Bronchospasm and should be avoided in cases of COPD
How do you treat he virus most likely to cause chronic hepatitis and Hepatocellular carcinoma?

1) IFN-a (flue-like symtpoms and depression)

2) Ribavirin- (Hemolytic anemia) needs intracellular phosphorylation and decreases GTP pool by inhibiting IMP-DH

3) Boceprovir (anemia and dysgeusia)- cleaves HCV NS3 protease

3) Beceprovir
What is the reservoir/transmission route of the non-enveloped ssRNA(+) virus that causes self-limited (12-48 hours) acute gastroenteritis with nausea, vomiting, diarrhea and abdominal pain
Norovirus (calicivirus)

1) Human reservoir
2) Transmitted oral-fecal and airborne fomites (vomiting)
What pathogens should be on the differential for Pneumonia?
1) Bacteria- Stre. pneumo and Atypicals

2) Viral- Influenza, Para-influenza, AV, RSV, Metapneumovirus
What is the reservoir/transmission of the virus that causes acute respiratory distress with a very short incubation time?
Sounds like SARS (corona virus- enveloped, ssRNA(+))

1) Bats are natural reservoir and regurgitate and poop out virus (CoV that adapted to human-human transmission)

2) Transmitted fecal-oral/urine
What is the major concerns with H5N1?
Avian Influenza

1) Lethality
2) Host range (antigenic shift between humans and birds)
3) Persistent in envelope (resistant to amantidine and rimantidine)
4) New reservoirs
What is the most common cause of prion disease?
Remember, prions are dead proteins

- Sporadic CJD

- Familial (10-15%) and Infection (1%) more rare.
What infectious disease causes encephalitis in Southeast Asia involving Bat-to-Pig-to-Human transmission?
Nipah Virus
What infectious disease causes Pneumonia in children and was identified by "PCR fishing"?
Which "Dengue-like" disease involves a mosquito vector and is epidemic in most of asia?
Which bugs most commonly cause HA-pneumonia vs. CA-pneumonia?
HA= Pseudomonas and Staph aureus

CA= Strep pneumo and H. influenza
What bugs should be on the differential for acute cystitis and pyelonephritis?
1) E. coli

2) Enterococcus faecalis

3) Proteus mirabilis

4) C. albicans.
What is the most likely cause of of vascular line-related bacteremia?
Staph aureus or Staph saprophyticus/epidermitus
Which bugs are most likely to cause encephalitis?

What about meningitis?
1) HSV and CMV, as well as WNV cause encephalitis

2) N. meningiditis, Listeria monocytogenes and Cryptococcus cause meningitis
What is the most common cause of infectious diarrhea?
Clostdridium dificile (A and B toxins that involve monoglucose transfer to rho proteins)
What are the most important causes of Urethritis?

What about Genital Warts?

1) Urethritis- think Chlamydia trachomatis and N. gonnorhea

2) Genital warts think HPV

3) Painless ulcers are Syphilis and Painful ulcers are HSV.
What bugs most commonly cause superfiscial cellulitis vs. abscesses?
Strep spp. in superficial.

Staph is abscessing.
A patient presents with CGD and neutropenia.

What is common about the organisms that this patient will be most susceptible to?
Catalase (+) organisms

1) Pseudomonas (also oxidase +)
2) Staph aureus (also coagulase +)
3) Aspergillus as well
A patient presents with an RES abnormality that causes a complement deficiency.

What is common about the pathogens that this patient might be particularly susceptible to?
Encapsulated organisms (also the case in IgG deficiency)

Strep. pneumo
Haemophilus influenza
N. meningitidis
What pathogens are most commonly seen in HIV-positive people?
1) Oral- candidiasis with thrush that may be esophageal

2) Respiratory- HSV-1/2, CMV, VZV

3) GI- Mycobacteria avian complex

4) Pulm- TB and P. jirovici

5) Neuro- Toxoplasma and Cryptococcus

6) Cancer- NHL and KS
Which in vivo, enterotoxin-producing bacteria is rare in that it is invasive?
Shigella dysenteriae
What are the 6 food-borne pathogens in order of frequency?
1) Non-typhoid Salmonella (invasive)
2) C. perfringens
3) Shigella (invasive)
4) Campylobacter jejuni (invasive)
5) E. coli
6) S. aureus
Which bacteria are invasive in the intestinal epithelium?
1) Non-typhoid Salmonella
2) Shigella spp.
3) Campylobacter jejuni
4) Listeria monocytogenes
5) Yersinia enterocolitica
What are the most common water-borne pathogens (Bacterial, Viral and Protozoan)?
Bacteria (Shorter incubation)= Vibrio cholera and other gram-negatives

Protozoa= E. histolytica, Giardia, Cryptosporidium

Viruses= Hep A, Norovirus, Rotavirus, Enterovirus
A patient presents with bloody diarrhea containing fecal leucocytes.

A blood sample comes back with motile, gram (-), oxidase (+), comma-shaped rods that are microaerophilic and grow at 42 degrees.

What is the pathogenesis of this pathogen?
1 day or so after exposure and lasts for 5 days

1) After ingestion, C. jejuni attaches to small intestine with adhesins and invades with LPS, causing inflammation

2) Sequele can include Guillain-Barre and Arthritis

**has enterotoxin that may not be important** (NOT FOR PATH)
A patient presents with explosive, foul-smelling diarrhea (devoid of blood) after drinking water 3 weeks ago in Africa.

Trophozoites were found in his stool

What is the reservoir/transmission and life cycle of the pathogen causing these symptoms?
This sounds like Giardia lamdia (longer incubation than Campylobacter). Treat it with Metranidazole

Wild Animal and Pet reservoir through water or fecal-orale

1) Trophozoites multiply in duodenum and prevent absorption

2) Infectious (only need 10!), Cl-resistant Cysts form in colon and are secreted in stool
A patient presents with prolonged diarrhea and oocysts are found in his stool that stain by modified acid-fast.

He is HIV positive, and you are particularly concerned about the severity of his dehydration.

What is the reservoir/transmission and life-cycle of the pathogen causing these symptoms?
Cryptosporidium parvum

1) Zoonotic reservoir spread by ingestion/contaminated water or person-to-person by fecal-oral.

- After INFECTIOUS, Cl-resistant oocysts are ingested, the develop into Sporozoites

- Sporozoites invade enterocytes and become trophozoites (May cause inflammation and malabsorption)

- Trophozoites divide into Merozoites, which can develop in oocysts that are shed in stool.
How can you treat a case of Cryptosporidium parvum?
If immunoCOMpetent, use Nitazoxanide

If suppressed with HIV, try ART or maybe paromomycin.
A 1 year old boy presents with severe diarrhea and dehydration in the winter time

Serology indicates the presence of viral RNA.

What is the pathogenesis of the virus causing these symptoms?
The age and diarrhea suggest Rotavirus, which is dsRNA, non-enveloped, acid-resistant virus and is MOST COMMON cause of infectious diarrhea in kids <2.

Transmitted human:human via fecal-oral and produces NSP4

1) After ingestion, virus multiplies in intestinal mucosa

2) 48 hours after infection, intense diarrhea and vomiting occur and last for 3 days-week.
How do you treat/prevent Rotavirus infection?
Most common cause of infectious diarrhea in kids <2

1) Live vaccine is not given to infants or immunodeficient.

2) Restore fluid/electrolyte balance.
A patients blood work comes back and is positive for anti-HAV IgM antibodies.

What is the pathogensis and reservoir/transmission of this virus?
HAV is a Picorna virus (non-enveloped ssRNA (+)) with a single serotype. No anti-viral, but can give IG if recent, or killed vaccine.

It is human:human with fecal-oral via food or water.

1) After ingestion, virus replicates in gut (50% of infected people have flu-like symptoms)

2) If insufficient Ab, HAV invades blood and goes to liver, where it causes acute inflammatory response (CTL-mediated)

3) 1% of systemically ill develop Fulminant Hepatitis, which can be fatal
Name 5 important ingestion-acquired pathogens.
1) Campylobacter jejuni
2) Giardia lambdia
3) Cryptosporidium parvum
4) Rotavirus
5) HAV
What are the important bacterial intoxications in order of incubation period (fast to slow)?
1) Staph aureus (1-6 hours)
2) Bacillus cerus (1-6 hours)
3) C. perfringens (12 hours)
4) C. botulinum (12-72 hours)
A 24 year old male presents with dysuria and urethral discharge.

He has epididymitis and is developing Reiter's syndrome.

What is the life cycle of the pathogen causing these symptoms?
Chlamydia trachomitus (gram-negative, obligate inctracellular, that lacks peptidoglycan and acts as an energy thief)

1) Infectious EB with disulfide linkages enters epithelium and prevents phagosome/lysosome fusion

2) EB reorganizes to form RB, which replicates by binary fission in endosome.

3) 48-72 hours later, RB becomes EB, and are released via exocytosis (Often asymptomatic!)
A 24 year old woman presents with PID, Urethritis and Cervicitis (with discharge).

What is the pathogenesis of the obligate intracellular pathogen that causes these symptoms?
C. trachomatous.

** look out for Fitz-Hugh-Curtis syndrome with the PID!

1) Serovars A-K infect and grow within epithelial cells of ocular and genital mucosa

2) Infected cells produce inflammatory mediators, which attract PMNs, NK and DC (HOST IMMUNE RESPONSE)

3) Recovery depends on Th1 response (CD4-MHC-II)

** No persistent immunity
A 24 year old woman presents with a small painless papule on her vagina.

She later develops a fever and inflamed LNs.

What type of Chlamydial infection might cause this?
C. trachomatous biovars L1-L3 cause LGV, which can also lead to Elephantiasis and LN rupture.
A baby presents with Conjunctivitis and Pneumonia (with Stacatto cough).

There is tachypnea and rales, but no wheezing.

What bug is infecting here?
Newborn Chlamydia trachomatous infection!
A 24 year old man exhibits painless chancre on his penis.

Under dark-field microscopy, you find tiny bacteria that lack LPS (they have gags instead) exhibiting corkscrew locomotion.

What is the timeline/pathogenesis of the pathogen causing these symptoms?
Treponema Pallidum (Primary Syphilis)

**fastidious, obligate intracellular pathogen**

1) Treponemes penetrate minor abrasion in skin or mucosal surfaces (or across placenta) and adhere to endothelial cells

2) Primary painless chancre develop after 3 weeks and last 2-6 weeks and treponemes spread hematogenously, adhering to vessels.

3) Asymptomatic period of 2-24 weeks

4) Secondary Syphilis (2-6 weeks) with mucocutaneous lesions on trunk, palms and soles (25-50%) and painless lymphadenopathy.

**Condula lata in 10% of patients**

5) Latent for 3-30 years in LN and spleen

6) Reactivation and Tertiary syphilis with Granulomatous Gumma on skin/bone/liver, Tabes dorsala, Neurosyphilis or Aortic lesions.
A 25 year old pregnant woman presents with painless vaginal chancre.

How do you confirm your expected diagnose and how might you treat?
sounds like primary Treponema pallidum (syphilus)

1) Diagnose with EIA-RPR-EIA

2) Treat with PCN (especially since she is PREGNANT!)
Which pathogens are transmitted via Zoonosis?
1) Hantavirus (rodents)
2) Rabies (animal bite)
3) Rickettsiae (dermacentor tick)
4) Borrelia burdorferi (ixodes tick)
A patient presents with fever, headache, GI distress and renal shutdown

They have been cleaning their house and report contact with rodent feces

What pathogen is causing these symptoms and what is the pathogenesis?
Rodent contact with fever and renal shutdown suggests aerosole-type infection with Hantavirus in HFRS form

- enveloped, ssRNA(-) virus with 3 distinct RNAs and two virally derived envelope glycoproteins

1) Envelope glycoproteins determine host range

2) Pathogen invades respiratory tract and spread hematogenously to many organs.

Remember, if you see neutorphilic leukocytosis, hemoconcentration and platelet deficiency, This Hantavirus Pulmonary Syndrome.
A patient presents with fever, headache, GI distress and hemoconcentration and thrombocytopenia

They have been cleaning their house and report contact with rodent feces

What pathogen is causing these symptoms and what is the diagnosis/treatment?
Sounds like Hantavirus Pulmonary Syndrome

- ssRNA (-), non-enveloped virus with 3 distinct RNAs and two virally derived envelope glycoproteins

- Diagnose by RT-PCR of viral RNA
- Treat with IV fluids/electrolytes and kidney dialysis if renal failure.
A patient presents with abnormal sensation surrounding a wound on their left distal leg and refuses to swallow liquids

They were recently bitten by a dog

What pathogen is causing these symptoms and what is the Pathogenesis?
Rabies Virus (ssRNA (-) that is "Large and bullet-shaped")

1) Animal bite gives virus access to muscle, where it spreads to peripheral nerve cells and CNS (up to 12 month incubation)

2) From CNS down peripheral nerves to other organs (Salivary glands) and leads to confusion, lethargy and increased salivation by inhibiting AchR

3) Seizure, Coma and/or Paralysis with death by respiratory failure.
A patient presents with abnormal sensation surrounding a wound on their left distal leg and refuses to swallow liquids

They were recently bitten by a dog

What pathogen is causing these symptoms and what is the the diagnosis/prevention/treatment procedure?
Rabies- ssRNA (-) that targets AchR with neuronal tropism

1) Diagnose with CLINICAL HISTORY or anti-rabies antibodies

-For pre-exposure immunization, give HDCV


- If they were previously vaccinated, clean would with virudical agent and give HDCV, but NOT IG

- If they were not vaccinated, clean, give HRIG and then boost vaccine.
What pathogen causes Rocky Mountain Spotted fever, what is its vector and what is the pathogenesis?
Rickettsia (obligate intracellular, gram (-) in Dermacentor ticks

**Treat with Doxicycline during early stages **

1) Ticks bite host in North and South America and 2-12 days later, fever, malaise, and severe frontal headache develops.

2) 2-4 days later, rash develops on extremities

1) Pathogen invades vascular endothelium, and directs actin reorganization to form filopodia for spread between cells.

2) Pathogens replicate intracellularly and make Phospholipases, Proteases and Membrane peroxidation damages endothelial cells and leads to capillary and small vessel rupture.

- Ticks bite host in North and South America and 2-12 days later, fever, malaise, and severe frontal headache develops.

-2-4 days later, rash develops on extremities
A 35 year old male presents with bright red bull's eye rash and he informs you that he was bit by a tick 15 days earlier.

What pathogen is causing this rash and how might the pathogenesis develop?
Borrelia burdorferi from Ixodes Tick (nymph or adult) requiring 48 hours of contact with human host.

1) Early dissemination (2 weeks- 6month) in 10% can cause neuropathy and meningitis, as well as AV block

2) Late dissemination (2 mos-7yrs) can cause Oligoarthritis, ECM lesions and demylenation/dementia
Which pathogen uses differential expression of plasmid-encoded Osps lipoproteins to influence host tropism?
Borrelial burdorferi (Lyme) depending on tick or human host.
What are the 6 Category A agents in terms of biodefense?
1) Bacillus anthracis
2) Variola
3) F. tularemia
4) Y. pestis
5) Arenaviruses (Lassa fever) and Filoviruses (Ebola, marburg)- VHF
6) C. botulinum
A gram stain comes back with non-hemolytic, non-motile, catalase (+), gram (+) rods in a "boxcar" pattern.

What virulence factors/pathogenesis is associated with this pathogen?
Bacillus anthracis

-pXO1 produces Edema Toxin (increase cAMP), Lethal Toxin (decrease MAPKK)

-pXO2 produces PGA capsule

- 95% cutaneous from injection drug use of drum skins, causing PAINLESS black eschar vesicles 1-7 days after

- Sporadic GI from uncooked meat has 40% mortality

- 5% Inhalation with flu-like illness, mediastinal widening and hemmorhagic meningitis, but NO rhinorrhea
How do you transmit/diagnose/treat the infection that causes painless, black eschars in its cutaneous form?
B. anthracis

1) Transmit through SPORES, NOT HUMANS

2) Diagnose with blood culture (6-24 hours)

- Treat cutaneous or post-expsure prophylaxis (also 3 doses of vaccine) with 60d Cipro or Doxi

- Treat GI or Inhalation with Cipro or Doxi with 2 others (resistance) and drain pleural effusion.

- Vaccinate with 5 doses.
How do you diagnose Lyme disease?
EIA (sensitive) followed by Western (specific)

Also true for HIV!
A patient presents with sudden-onset fever, chills and and malaise. You also notice ulcers and tender lymphadenopathy.

The gram stain comes back with very few gram (-) coccobacilli.

What is the reservoir/transmission/treatment of the pathogen that causes these symptoms?
Francicellsa tularensis (need Cysteine to grow)

- Many modes of entry (especially dogwood and lonestar ticks) but NOT PERSON:PERSON

- VERY VIRULENT (like Giardia) with FPI and capsule

- Streptomycin or Doxicycline (especially prophylactic) X 14 days
A patient from the southwest US presents with acute febrile lymphadenitis, Pneumonia and Septicemia.

Blood culture comes back with gram-negative bacilli staining in a "bi-polar" fashion.

What is the virulence factors/pathogenesis of the pathogen that causes these symptoms?
Y. pestis (droplet contagious for 72 hours)

1) Plasminogen activator (coagulase in flea mid-gut), Outer protein virulon (Type III) and LPS

2) Flea picks it up from rodents, can't digest it and then passes it to humans (CONTAGIOUS droplet for 72 hours)
How would you treat/prevent a case of bubonic plague?
1) Streptomycin or gentamicin X 10 days or Doxi

2) Doxi or Cipro for 7 days (same as Tularemia)
A patient presents with a centrifugal rash and many pustules on their body.

How do you prevent/treat the condition causing these symptoms?

1) Vaccine given 4 days after exposure or to prevent, but not in Immunodeficiency, Eczema or Pregnancy because of Eczema vaccinatum, Progressive vaccinia and Post-vaccinia encephalitis.

2) Treat with Cidofovir
Which viruses cause viral hemmorhagic fever and how do you treat them?
**USE up coagulation factors and you bleed!**

1) Filovirus (Ebola and Marburg) and Arenavirus (Lassa fever)

- cause high fever and vascular damage through contact with blood and body fluids from RODENTS.

2) Only treat Lassa with Ribavirin
A patient presents with bilateral symmetric descending acute paralysis.

How do you treat the pathogen causing this symptom?
C. botulinum

Antitoxin and supportive care.
Which bacteria are motile?
Vicky Can Learn To HELP Bake Cakes Slowly

1) Vibrio cholera
2) Chlamydia
3) Listeria (tumbling)
4) Treponema pallidum (corkscrew)
5) Heliobacter Pylori (corkscrew)
6) E. coli
7) Legionella
8) Pseudomonas
9) Borrelia burdorferi
10) Campylobacter jejuni
11) Salmonella
A 60 year old patient with COPD presents with night sweats, hemoptosis and dyspnea. He is also cachexic.

How do you confirm your diagnosis and how might you treat?
This sounds like TB.

Remember, these bacteria are small enough to get into the lungs, but big enough to stay in the aveoli.

1) Do an acid-fast stain for M. tuberculosis (70% sensitive)

- Follow up with automated liquid culture (9 days for smear + and 16 for smear -) or Direct PCR (60% for smear -)

2) Treat for 2 months with RIF/ISO/PZA/ETH
Follow up with RIF/ISO for 4 months
A 60 year old female alcoholic patient with a positive acid fast stain and hemoptosis has ALT>3x normal

How might you adjust your drug regiment for this case?
This sounds like Anti-TB drug-induced Hepatotoxicity

- Age, gender and alcohol are risk factors

- Take her off PZA, then INH, then RIF. Adjust according to symptom progression (you can give non-hepatotoxic drugs).
A patient presents with a CNS injury that has damaged the innervation of the airway.

What types of infections are you concerned about?
Airway= Inhalation acquired, and this type of injury is predominately a concern for ENDOGENOUS flora

1) Anaerobic streptococci, Fusobacterium....Aspiration pnuemonia
Which pathogens are primarily inhaled?
1) Legionella (legionaire's pneumonia)
2) Tuberculosis
3) Pulmonary anthrax
4) Histoplasma (looks like TB from bird droppings)
5) Tularemia (pneumonia from rodents through ticks)
A group of 20 men and women with HIV present with upper respiratory features and gastroenteritis.

What is the pathogenesis of the pathogen causing these symptoms?
Epidemic + Immune Compromise = Adenovirus (linear, non-enveloped dsDNA virus)- DIAGNOSE with PCR!

- Fiber type dictates specificity and serotypes 40 and 41 are typical for for Gastroenteritis.

1) Virus binds to local epithelial/lymphoid cells (either aspiration, which is MOST SEVERE, or inhalation) via CAR and undergoes endocytosis.

2) Following endosomal acidification and lysis, virion DNA is incorporated into host.

3) Early genes E1A/B (inhibit host mRNA translation in nucleus), E3 (block host immune response in cytoplasm)

4) Cytopathic effect occurs and virions are released.
A 1 year old amish boy presents with fever of 104, lethargy and neck stiffness. He has not be immunized.

What is the pathogenesis of the pathogen causing these symptoms?
Toddlers + Lack of Immunization= Haemophilus Influenzae (SMALL, gram-negative coccobacilli that must be grown on chocolate agar)

- Vaccine against encapsulated strains (Hib) is effective when used.

1) In absence of protective Ab, droplets from infected or carriers colonize host
- LOS (adhesion/inflammation)
- Adhesins, Pili,
- IgA protease (immune avoidance)
- Iron uptake (metabolic)

2) In the presence of a viral infection or defect in humoral immunity, colonizing bacteria infect either LOCALLY (unencapsulated) causing OPS, or SYSTEMICALLY (encapsulated) causing bacteremia and meningitis.
What virulence factors are associated with small, gram-negative coccobacilli that must be grown on chocolate agar (Diagnosed with Gram Stain and Culture)?
**PRP CAPSULE in Hib**

1) LOS
2) IgA protease
3) Pili and afimbrial adhesins (like HA in pertussis)
4) Iron uptake from host
5) Genetic transformation
A 37 year old female presents with a persistent cough, erythema multiforme and anemia.

What is the pathogenesis of the pathogen causing these symptoms?
Persistent cough + Erythema multiforme + Anemia= Mycoplasma pneumonia (tiny with no cell wall and sterols in cell membrane) which is seen primary in ADULTS

1) Droplets colonize nasopharyngeal surface with Adhesins

2) Aspiration induces bronchopneumonia involving P1 adhesin, Peroxide generation, CARDS toxin and Inflammatory response
A 37 year old female presents with a persistent cough, erythema multiforme and anemia.

How do you confirm your diagnosis and treat?
1) Diagnosis of M. pneumonia is a problem with 70-90% symptomatic! Presents as interstitial pneumonia and USE PCR

2) Treat with agents that target Ribosome (tetracyclines and macrolides) and DNA (FQ), but EVIDENCE IS LACKING

In outbreaks, use azithromicin for prophylaxis.
What are the 3 important blood-borne pathogens?
Hep B (with or without D) (30%), Hep C (3%), HIV (0.3%)
What is the pathogenesis of the only enveloped, circular, incompletely dsDNA virus?

How do you diagnose chronic vs. acute cases?
Hepadna virus being Hepatitis B

1) Enter via blood or infected mothers and replicate in liver cells (80% subclinical, 20% with acute hepatitis, 1% with Fulminant)

- Damage occurs through cell-mediated host immune response (HBsAg is immune decoy

- Chronic in 2-10% of neonates and 90% of adults, which can lead to cirrhosis and HCC (HBx protein)

2) Anti-HBs Ag means acute resolved or vaccinated (NOT CHRONIC)

HBsAg means acute or chronic (if persistent)

Anti-HBc Ag can be chronic but NOT ACUTE
A patient presents with elevated liver panel enzymes, HBsAg and Anti-HBcAg.

How do you treat?
This is chronic hepatitis B

Treat with Peg-INF-a and Lamivudine
True or False.

Hepatitis D involves a direct cytopathic effect on the liver, while Hepatitis B is indirect.

HepB is immune-mediated
HepD is direct
How do you diagnose/treat the liver disease caused by an enveloped ssRNA (+)?
Hep C (very heterogenous in blood- quasispecies)

**chronic infection with HCC most common, but less likely to be acute or transmitted than B**

1) Diagnose with RT-PCR
2) Treat with PEG-IFN-a, Ribavirin and Boceprevir

**Most responsive with IL-28 genotype= personalized M**
Which pathogens are at risk for re-activation in a transplant?
Primary infection is usually more severe

1) CMV

2) EBV (PTLD....lymphoma)

3) T. cruzi
What is the pathogenesis/treatment of the pathogen that causes PTLD?
EBV is immunosuppressed patients

1) Saliva to pharyngeal epithelium and tonsillar B cells (primary replication)- acyclovir during acute but not latent

2) Spread in blood to B cells and goes latent (can still be shed)

3) In immunosuppressed states, CTL cannot recognize latent EBV antigens and causes hyperplasia and lymphoma- DECREASE IMMUNOSUPRESSION
How do you diagnose the member of the Herpes virus family that binds to CD21 receptors?
EBV (enveloped, dsDNA virus)

1) Monospot to test for Ab during acute infection
2) EIA for chronic Ab and Ag.
3) qPCR for viral load and risk of PTLD
Which bacteria are gram-negative rods that are also oxidase-negative, facultative anaerobes which grown on MacConkey agar?
Enterobacteria, which can acquire virulence genes and cause opportunistic inections.

1) E. coli (Lac+)
2) Shigella (non-motile, H2S -)
3) Salmonella (motile, H2S +)
4) Y. pestis
5) Klebsiella
6) Proteus
Which E. coli strain has each of the following characteristics?

1) LT (like cholera at Gs), CFA pilis and STa

2) Hyl, LPS and bundle-forming pili, intimin

3) Shiga toxin, intimin, Endotoxin

4) Type 1 pilin, Endotoxin

5) Biofilm, EAST
1) ETEC (not invasive, watery diarrhea in travelers)
2) EPEC (pediatric diarrhea with A/E lesions and pedestal)
3) EHEC (HUS in children through meat and zoo)
4) EIEC (invasive, like shigella in lytic effects)
5) EAEC (adhere in biofilm and watery diarrhea)
How does EPEC and EHEC gain access to cells (poorly invasive)?
1) BFP (EPEC) or Type 1 pillus (EHEC) bind enterocyte

2) Type III secretion of TIR to host cell followed by intimin binding

3) Pedestal formation and close association with enterocytes leads to diarrhea
What is the most common cause of CA-UTI vs. HA-UTI?
CA-UTI is 80% E. coli and 20 % other enterobacteria

HA-UTI is 20% E. coli and 80% other enterobacteria
What E.coli infection should never be treated with antibiotics?
HUS from EHEC (they are in renal failure).

Treat UTI with nitrofurantoin and neonatal meningitis with Amino-penicillin or other suitable choice with CNS distribution.
What is the virulence/pathogenesis of gram(-) rods that are microaerophilic, motile and grow at 37 and produce urease to raise pH.
H. pylori (C. jejuni would be at 42)

1) Colonize GI and cause mild disease (Urease and Flagella avoid gastric pH issues)

2) Duodenal/gastric ulcers develop in 1% (VacA, LPS and CagA damage stomach eipthelium (cag pathogenicity island encoding IV secretion system))

3) A few get gastric cancer
If you see gastric/duodenal ulcers, how might you diagnose/treat the expected pathogen?
Sounds like H. pylori

1) Biopsy and gram stain or Breath test with radioactive urea

2) Combination therapy with Macrolide and Omeprazole (acid blocker)- 90% effective
What are the most common causes of the most common Nosocomial infections?
** C dif. diarrhea**

1) Blood-borne (Enteroccus, S. aureus

2) UTI (non-E. coli enterobacteria are 80%, Enteroccus)

3) Pneumonia (Pseudomonias and Staph)
Match the Nosocomial pathogen with its Virulence factors/pathogenesis or clinical manifestation

1) Toxin A, Toxin B and with rho-glucosylation
2) Hematogenous endocarditis and UTI
3) Skin abscesses
4) Ascending anal infection with aspiration VA-pneumonia
5) Mucoid nature resists phagocytosis
6) Uncommon wound/bloodstream infection
1) C. dif (Diarrhea..pseudomembrane..toxic megacolon)
2) Enterococcus (gram + cocci)- Linezolid/Daptomycin
3) CA-MRSA- Bactrim
4) Klebsiella
5) Klebsiella- Carbapenem or Polymyxn if necessary
6) Acinetobacter
What bugs require droplet precautions?
1) Meningococcus
2) Influenza
3) Pertussis
4) Mumps and Rubella
Which pathogens are invasive?

Important examples include ENTEROPATHIC Yersinia spp and Shigella/Salmonella

**Those that stop in epithelium exert effects more quickly than disseminated**
How do Y. enterocollitica and Listeria (blood-borne in leukocytes) invade the colonic epithelium?
** Can transfer 1 of 3 invasive genes to E. coli to make it invasive!**

1) Invasin (made at low temp) binds B1 integrin on M cell in colonic epithelium causing "zipper" adherence

2) Following endocytosis, pathogen is released to Peyer's patches in sub-epithelium and either stay or go to LN

3) (Yersinia) After ingestion, LPS causes fever and YOPS resists phagocytosis
You diagnose shigella by fecal leucocytes and culture on MacConkey agar.

How does Shigella invade the colonic epithelium?
Need 30 genes vs. 1 gene for Y. enterocolitica

1) Body temp triggers gene expression including TTSS (III) needle secretion system (Mxi-Spa proteins)

2) TTSS transfers IpA (Sip if salmonella) to host cell surface, causing membrane ruffling

3) Macropinocytosis occurs Shigella is transcytosed and picked up by macrophages, which it lyses.

4) Enter macrophages on basal side of colonocyte and uses Ipa to get into second colonocyte and escape into the cytoplasm

5) IcsA enables cytoplasmic movement through actin polymerization

6) IcsB enables pathogen to get to next colonocyte and escape double-walled vesicle without exposing to extracellular environment.

7) Shiga toxin causes Gi symptoms and fever
Which pathogens that we have talked about are PARTICULARLY virulent in low numbers?
1) Francicella tularermia

2) Giardia lambdia

3) Shigella dysentaria

4) Toxins
Which pathogen uses a Serotype B polysacharide capsule to mimic human neuronal sialic acid?

Which pathogen uses a hyaluronic acid capsule?
1) Serotype B/Sialic acid capsule is for N. meningitidis (meningitis and meningococcemia

2) Hyaluronic acid capsule is Strep A (pharyngitis, bacteremia, toxic shock
How does T. cruzi cause neural damage?
Autoantigen response with cross-reactive peptides that activate B cells.

Also Chagas disease in South America, with esophageal and colonic dysmotility from kissing bug
Your patient is a doctor who has been treating young children in Subsaharan African.

He exhibits high fever, Petechiae/Purpura, hypotension, headache and a stiff neck.

A gram stain comes back with gram (-), oxidase (+), non-motile dipplococci.

What is the pathogenesis of the pathogen causing these symptoms?
This is N. meningitidis (SS Africa and youth are carrier risk factors)

it is COmPLICated
(complement-binding protein, OMP, Pili, LOS, IgA protease, Capsule)

1) Colonize respiratory tract using OMP and Pili

2) IgA protease inhibits opsonization through fabulation and complement-binding proteins bind up factor H

3) Invade epithelial cells and lose sialic acid capsule

4) Within vascular space, release LOS and circulate to brain, skin (purpura), joints (arthritis) and bones (osteomyelitis)
Your patient is a doctor who has been treating young children in Subsaharan African.

He exhibits high fever, Petechiae/Purpura, hypotension, headache and a stiff neck.

How do you diagnose/treat the pathogen causing these symptoms?
This is N. meningiditis (young, SS Africans are carriers)

1) Diagnose by CSF gram stain and look for gram-negative dipplococci that are OXIDASE(+) and that ferment maltose.

2) Treat empirically with Ceftriaxone or high dose PCN.

- Vaccinate with conjugate MCV4!!!! (only leaves serogroup B, which is a problem for infants)
A patient presents with pharyngitis

Blood work comes back with gram(+) cocci that are PYR-positive and beta-hemolytic on blood agar.

What is the pathogenesis of this organism?
This is Strep pyogenes (if Bacitracin sensitive)

Causes, Mucosal (pharyngitis), Pyogenic (Nec fasc), Toxigenic (TSS) and Immunology (Rheumatic fever) disease.

1) For pharyngitis and Pyogenic infection, bacterium attaches to oropharynx with M protein and LTA

2) Exotoxin production ensues, with Hyaluronidase (matrix digestion), Hemolysin (RBC) and Streptokinase (Prevents coagulation after leak)

3) Immune response will clear pharyngitis, but not Pyogenic or other deeper infections.
What pathogen causes Scarlett fever and how? What virulence factors does it possess?
Strep pyogenes with Erythrotoxin**, M protein, Hyaluronic acid capsule, LTA, IgA protease, Hyaluronidase, Hemolysin, Streptokinase and C5a peptidase.

1) GAS colonizes mucosal surface of throat or wound with LTA and M protein and produces toxins.

** Also the cause of toxic shock syndrome
How do you diagnose/treat the pathogen that causes Hematuria (coca cola urine), Edema and Hypertension?
Post-streptococcal glomerulonephritis (PSGN) from GAS

MUST CULTURE for B-hemolysis, PYR and bacitracin.

Can prophylactically use PCN for rheumatic fever.

Treat with Amoxicillin.
Which pathogens produce IgA protease?
Remember, IgA protease uses fabulation and is for extracellular pathogens that don't want to be phagocytosed

1) Strep pneumo
2) N. meningitidis
3) N. gonorrhea
4) Haemophilus influenza
What 2 toxins cause toxic shock syndrome and through what organisms?
1) Erythrogenic toxin from Strep A

2) TSST-1 from Staph. aureus.
Which two pathogens have polypeptide capsules?
1) B. anthracis (PGA)

2) Y. pestis

Others are polysacharide (Some Crazy Students Have Not Bathed Since Passing the Kidney Exam)

StrepA, Cryptococcus, Salmonella typhi, Haemophilus 1b, influenza, Neisseria meningitidis, Bacillus anthracis, Strep pneumo, Pseudomonas, Klebsiella, E. coli
A 69 year-old male with COPD presents with a fever, dyspnea, chest pain, rigors and thick, yellow sputum.

Gram stain shows catalase (-), gram (+) dipplococci that are alpha-hemolytic.

What is the pathogenesis of the bug causing these symptoms?
Strep pneumoniae (carried in URT) causes MOPS

1) Respirated droplet colonizes upper respiratory tract with Neuraminidase and IgA protease

2) In absence of Ab (Hyaluronic acid capsule) or during viral co-infection, it may move to lower airway by aspiration, cause local infection or enter the bloodstream

3) Inflammation (LTA promotes IL-1 and TNF-a) and Bronchial damage (pore-forming Pneumolysin)
What is the underlying cause of each of the following symptoms in a Strep pneumonia infection?
1) Fever= LTA and pneumolysin
2) Dyspnea= Inflammation and debris in alveoli
3) Chest Pain= Infection of parenchyma inflames pleural lining
4) Cough: Fluid in alveoli
What types of resistance occur in the most common cause of CA-pneumonia?

How do you prevent this type of disease?
Strep pneumonia

1) Altered PBP (just add more)
2) No beta-lactamases

PCV13 conjugated vaccine (similar to haemophilus influenza 1b)
A patient presents with what she calls a "spider bite." It has developed into an abscessing infection.

You drain it and find clusters of gram positive cocci in a blood sample.

What virulence factors are associated with this pathogen?
S. aureus (probably CA-MRSA) person:person from fomites NOT DROPLET

**Worry about Toxic shock, Central venous catheter (because of clotting factors) and Abscesses.

1) Exotoxins
- Many Hemolysins
- Many Enterotoxins
- Exfoliative toxin A and B (scalded skin)
- TSST-1

2) Adherence
- Protein A (Fc of IgG to stop opsonization)
- fibrinogen, collagen, fibronectin binding molecules

3) Cell Wall
- Peptidoglycan (cytokine release)
- LTA (inflammation)
- Unimportant capsule
What is most likely to be affective against a CA MRSA infection?
Clindamycin (but look out for C. dif).
Which pathogens exhibit antigenic shift vs. drift?
Drift= Influenza, Rhinovirus, HIV

Shift= Influenza, N. gonnorhea, T. brucei
What is the pathogenesis of the segmented, enveloped ssRNA(-) virus that exhibits antigenic drift (seasonal) and shift (Pandemic)?
Influenza (A is major)

1) Droplet is inhaled and HA-mediated binding and fusion occurs

2) HA is cleaved by host protease into HA1 and HA2 and virus is endocytosed (HA2 allows gene segments to enter cell for replication)

3) NA critical for viral aggregation and release.
What types of antigenic variation occur in the gram (-) dipplococci that do not ferment maltose?
N. gonorrhea

**1) Antigenic and Phase variation through GENE CONVERSION in Pilus with pilE expression site and pilS variable regions (1-6 copies)

**pilS can come from other bacteria through transformation**

2) Phase and antigenic variation in Opa proteins (increase adherence to host)
3) Phase and Antigenic variation in LOS (inflammation)
What types of antigenic variation and pathogenesis occur in the flagellated protozoa that travels in the "tsetse fly" in Africa?
T. brucei causes chancre at bite (Stage 1) followed by lymphoadenopathy and systemic spread leading to CNS involvement (sleeping sickness and meningoencephalitis)

1) Antigenic variation (survive against Ab in blood) through GENE CONVERSION in VSG of extracellular parasite (homologous recombination of silent sequences)

2) Epimastagotes multiply in the salivary gland and become Metacyclic trypomastigotes, which are taken up by fly.

3) In next human, metacyclic trypomastigotes become Trypomastigotes in bloodstream, which multiply by binary fission.
Which protozoa has an intracellular stage called "amastigote" and causes GI dysmotility?

What is the significant of this?
Trypanosoma cruzi in "kissing bug" from South America.


Unlike, T. bucrei, which has only blood-borne trypomastigote stage, T. cruzi has both trypomastigote and amastigote stages.
What are the major intracellular pathogens?
Gain access through Invasins and/or Phagocytosis

1) Listeria monocytogenes (Escape vacuole)

2) Legionella pneumophila (prevent phag/lys fusion)

3) Plasmodium faciparum
How does CMV avoid immune recognition by the host T-cell response?
1) Interferes with CTL by down-regulating MCH-I by messing with Tap.

2) Interferes with CD4+ response by down-regulating MHC-II
How does the catalase-positive, oxidase-negative, gram positive rod that is found in processed foods avoid immune recognition when invading epithelial cell?
Listeria (neonatal meningitis)- Escape to Cytoplasm


1) Taken up by phagosome and acidification triggers listeriolysin (hlyA) to break open phagosome

2) Forms actin "tail" (actA) that allows cell-to-cell spread without exposure to extracellular environment

3) PLCb allow listeria to exit from double-walled vesicle in second cell (like IscB in Shigella)
What is the reservoir/transmission/diagnosis/treatment of the pathogen that is the primary cause of neonatal meningitis?
Listeria monocytogenes (along with group B strep and E. coli)

1) Naturally found in soil

2) Food-borne transmission in processed foods and soft cheeses

3) Diagnose with monocytes in CSF smear (gram stain is not reliable

4) Treat empirically with Ampicillin or Bactrim
What are the 3 bugs that cause neonatal meningitis?
Listeria (#1), Group B Strep, E. coli
A 60 year old man with a history of smoking presents with cough, fever and diarrhea. You suspect pneumonia, but your gram stain in negative. The pathogen grows on Charcoal yeast and a Urinary Antigen test confirms your diagnosis.

How does the pathogen causing this pneumonia avoid immune recognition when invading epithelial cell and how might you treat?
This is gram-negative Legionella= Prevent Phago/Lyso fusion

Cl-tolerant in water..mostly biofilm in cooling towers or Amoeba.

1) Ingested by phagosome and dot/icm (IV) "modulate" phagosome to inhibit lysosomal recognition (makes it look like ER)

2) FQ and Macrolides (3-5 days to take effect)
A 40 year old man who was recently traveling in Africa presents with cyclic fevers, headache, dark urine and a lower lobular crackle.

What is the pathogenesis of the organism causing these symptoms?
Plasmodium falciparum

1) Sporozoites in mosquito become tissue Schizonts in the liver and transform into Merozoites

2) Merozites go into RBCs (Ring, trophozoite, schizont) causing fever cycle.

3) Schizonts in blood can become Gametocytes
What is the difference between the protozoan life cycle of Plasmodium faciparum and that of Vivax or Ovale?
1) Vivax/Ovale have Hypnozoites in latent liver stage (temperate climate)

2) Ring in merozoite stage is specific to Falciparum (tropical)
What virulence factors does P. falciparum have and how do you treat?
1) PfEMP expression causes "knobs" on parasatized RBCs, which allow binding and sequestration, leading to vascular obstruction to perfusion

2) If blood smear is positive for parasite:

- use Primaquine for liver stage in Ovale/VIvax
- either Mefloquine or Atovaquone/proguanil for chloroquine-resistant Falciparum forms
Which toxins increase cAMP leading to secretion of fluid?
1) Cholera toxin and LT from ETEC (ADP-ribosylates Gs)
2) Pertussis toxin (ADP-ribosylates Gi to inhibit it)

**STa in ETEC and Y. enterocolitica increases cGMP to inhibit absorption**
Which toxins inhibit protein synthesis?
1) Shiga toxin and Shiga-like toxin cause HUS by binding 60S rRNA subunit and inhibition translation

2) Exotoxin A (Pseudomonas) and Diphtheria Toxin (Corynbacterium) bind to eIF2 and inhibit elongation of protein.
Which toxins act on the CNS to cause paralysis and how?
**Both are proteases that act on vesicle docking

1) C. botulinum (flacid)- Botulinum toxin inhibits Ach release at NMJ

2) C. tetani (spastic)- Inhibits Glycine/GABA release at spinal chord.
Which toxins act on the cell membrane (Hemolysin)?
**Affect WBC and RBC

1) Streptolysin/Listeriolysin

2) Pore-forming alpha toxin (Staph aureus, E. coli/UTI, C. perfringens))
A 34 year old male with severe burns presents with greenish discoloration on his burn dressing.

Gram stain comes back with gram (-) rods that are motile and oxidase positive.

What are the virulence factors of the pathogen causing this symptom?
Pseudomonas aeruginosa (opportunistic extracellular)

** Watch out in burn and CF**

1) Exotoxin A inhibits p-synthesis and causes necrosis
2) Enzymes cause tissue damage
3) Leucocidin kills WBCs
4) PLC is a hemolysin
5) Endotoxin causes shock
6) Slimy capsule contributes to CF
7) Pili
A patient is PPD+, but shows no pulmonary symptoms.

He wants to know whether he is dangerous to his children. What do you tell him?
1) TB does not have to be pulmonary!

2) If there are NO signs at all, the infection is probably latent (calcified granuloma), and he is there NOT INFECTIOUS
What are the virulence factors of M. tuberculosis?

What are the primary differences between M. tuberculosis and M. leprae?
Aerosolization, alveoli, parenchyma, LN, T cell response.. granuloma

1) Mycolic acids (isoniazid)
LAM (like LPS), Lipids
ESX secretion system (ESAT-6/CFP-10 for diagnosis)

2) Transmission, Growth in Lab, Capsule

- Can be grown
- No capsule

- Leprae
-CANNOT be grown
-Extended exposure
-PGL-1 capsule
How does M. tuberculosis bacteria evade immune recognition by the host?
Enter alveoli through aerosolization and goes to parenchyma (NOT AIRWAY)

1) Inhibit phag/lys fusion (like Legionella) and acidification

2) Catalase prevents oxidative burst effects (RNI are toxic to TB)

3) Down-regulates MHC-II (lipoprotein binds TLR-2 on chronically infected macrophages)
How do you diagnose a case of TB?
1) Clinical include night sweats, cough and dyspnea with cavity on X-ray

2) Acid-fast and PPD to determine Mycobacterium

3) IFN-y based (IGRA) to determine TB specifically

- EIA for ESAT-6/CFP-10

4) Gene expert machine is faster than traditional culturing.
Which pathogen infects Macrophages and induces a Th1 response which leads to granuloma formation?

How do you treat/prevent the disease caused by this pathogen?
1) M. tuberculosis- inhibits macrophage activation

Th1 (INF-y, TNF-a and IL-12) is important with CD4 T-cells, but CTLs may also play a role in recognizing infected macrophages

2) BCG is good vaccine in childhood TB (but not very good overall). Can give isoniazid 9 months after infection to prevent re-activation.

- R (DdRp) I (Mycolic acids) P (?) E (Cell wall)
- Second line drugs include Moxifloxacin
What is the difference between MDR and XDR TB?
Resistant forms of TB

MDR (2 frontline drugs, Rif/Iso)
XDR (MDR + >3 second line drugs)
A patient presents with sensory nerve damage to the fingers and toes.

Their blood work comes back with a positive acid-fast stain, low bacterial load, lymphophilia and you notice granulomas on a biopsy.

What is the pathogenesis of this disease?
This sounds like Tuberculoid Leprosy (high T cells, granulomas and low bacterial load).

- Less severe than Lepromatous and governed by Th1 response (DTH+ to lepromin) with IL-2 and IFN-g cytokines

- Inflammatory response causes nerve damage
- 90% of cases in India and Africa, but 10% in Mexico!
A patient who recently spent time in Mexico presents with thickened dermis and peripheral nerve enlargement/damage

CBC shows high bacterial load and lymphopenia

What is the pathogenesis of this disease and how do you treat?
Lepromatous Leprosy- Look out for Erythema Nordosum with immune-complexes!)

1) DTH-, CD8 dominated response with Th2 profile (IL-10, IL-4) favoring an antibody response (useless antibodies!).

- Only 10% of cases in India and Africa, but 90% in Mexico

2) Treat Leprosy with Dapsone and Rifampin (1.5-2 years)
Treat ENL with steroids

**Nerve damage is irreversible**
What Mycobacterium causes each of the following:

1) Necrotizing toxins to skin (Buruli ulcer in Africa and Aust)
2) Swimmer's granuloma
3) Pulmonary symptoms in HIV patients.
1) M. ulcerans
2) M. marinum
3) M. avium-intracellulare
What pathogen should be worried about if you have CF?

What about after a Splenectomy?

1) Pseudomonas

2) No IgG or complement so encapsulated Strep (C3)/Staph/Haemophilus/Neisseria (MAC)

3) Aspergillus (also staph and pseudomonas)
Which pathogens are the true opportunists?
1) Aspergillus
2) Cryptococcus (meningitis/Amphotericin-flucytosine)
3) Pneumocystis jirovici (pneumonia/Bactrim)
4) Candida albicans
An HIV positive patient comes in complaining of confusion and severe headache. He has a cat.

A CT reveals cysts in his brain.

What is the pathogenesis/diagnosis of the bug causing these symptoms?
Toxoplasma gondii (crosses Placenta!)

**Diagnose with ocular/CNS abnormalities- look for ring-like cysts in brain.

1) Infectious Sporozoites in cat feces are ingested (or latent Bradyzoites in meat) and penetrate intestinal wall

2) Tachyzoites live in macrophages and can disseminate to the fetus (congenital) or brain (Bradyzoites/Cysts)
or become gametocytes
What are the lifecycles of T. brucei, T. cruzi, T. gondii, P. falciparum and P. ovale?
1) T. brucei
-Epimastigotes (Salivary gland)
-Metacyclic trypomastigotes (fly)
- Trypomastigotes (multiply blood)

2) T. cruzi is same but with intracellular "amastagote" stage

3) T. gondii
- Infectious Sporozoites in cat feces or Bradyzoites in meat
- Tachyzoites in macrophages
- Congenital disease or Bradyzoites in brain cysts.

4) P. falciparum
- Sporozoites in mospquitto
- Tissue Schizonts in hepatocytes
- Merozoites in blood (ring..merozoite..schizont)
- Gametocytes to replicate

5) P. ovale also has hypnozoite stage latent in liver, but no right structure in fever stage.
Your patient presents with fever, malaise and lack of appetite, as well as dyspnea. PPD is negative.

On X-ray you discover a lower lobe infiltrate.

BAL is positive on Gomori silver stain (negative for Histoplasma and Blastomyces). He is from Arizona

What is the pathogenic life-cycle of the pathogen causing these symptoms
Dismorphic Coccidioides fits (Southwest and pathogenic fungus).

1) Mycelial form in soil is Infectious (wind disrupts hyphae)

2) Airborne spores enter respiratory tract and become Spherules

3) Spherules rupture and release endospores which form more spherules (NOT INFECTIOUS)- no human:human
Which pathogens lead to local pneumonias and which pathogens can interstitial pneumonia (X-ray findings)
1) TB and Coccidioides show lobular (sometimes cavitous) infiltrates.

2) PCP, Histoplasma are interstitial
How can you tell whether a C. albicans infection is cutaneous or disseminated by CBC?
PMNs mean disseminated

T-cell mean cutaneous
If your patient is traveling, which bugs are the major PRIORITY to prevent?
1) HepA & HepB (inactive vaccines)

2) Rabies (inactive) and Yellow fever (live)

3) Typhoid fever and Influenza

4) Meningococcus, Jap encephalitis
Which bugs do you treat empirically but NOT prophylactically in travelers?

1) Giardia lambdia (Metronidazole)
2) E. coli (Amoxicillin, Azithromicin)
3) Norovirus (good luck)
What drugs should traveler's take prophylactically when visiting friends and relatives (VFR) in SE Asia and Africa for 6 days?
Malaria is the concern here!
Malarone (Atovaq/prog) with food!

1) Chloroquine has resistance

2) Doxicycline is CHEAP, but takes daily for 4 weeks

3) Mefloquine (Lariam) is $$ per pill, but take WEEKLY for 4 weeks.

4) Atovaq/Prog (Malarone) is taken daily for 1 week ($$$ but cheaper for <7 days)
Your patient is traveling to Brazil and Argentina. How do you prepare them?

They are planning a trip to India later that year. What about for that trip?

1) Argentina and Brazil are concerning for Yellow Fever (vaccinate with live vaccine)

2) Typhoid fever (50-70% coverage for vaccine for 5 years)

3) Malaria and Meningococcal
Which bugs do you treat with Ribavirin?
1) Hep C (with IFN-a and Boceprivir)

2) Lassa Fever (Arenavirus)

3) RSV in infants (pnumonia)

4) SARS (coronavirus)
What pathogens are associated with each of the following areas?

1) Boat in Borneo
2) Lake in Malawi
3) Beach in Bermuda
4) Camp in Cambodia
5) Bing in Bangkok
6) Mexico
1) Leptospirosis
2) Schistosomiasis
3) Cutaneous larva migrans
4) Jap encephalitis
5) Hep A, E, Typhoid
6) Lepromatous Leprosy and Histoplasmosis
What are the incubation times for Malaria, Typhoid fever and VHF?
3 of 4 most URGENT (third is amebic liver abscess)

1) Malaria (7-90 days)
2) Typhoid (7-21 days)
3) VHF (2-21 days)
What OI do you see in HIV?
1) Mouth- Candida (thrush can go to esophagus)

2) Respiratory- TB (RIPE), PCP (bactrim)

3) Cutaneous- HSV-1/2 (acyclovir), VZV (acyclovir)= PAIN

4) GI- M. avian complex (macrolide, aminoglycoside)

5) Neuro- Cryptococcus (AmpB/flucy/flucon), Toxoplama (sulfa/pyrimethamine)

6) Malignancy- KS/HSV-8, NHL/EBV
What OIs do you see in HIV if CD4<200?

What about <100

What about <50?
1) <200 you see PCP
2) <100 you see Toxo
3) <50 you see MAC and NHL (EBV)
What NRTIs are available for HIV?
What NNRTs?
What PIs?
What Integrase
Use 2 NRTI with 1 from another class

1) Lets All Take Emily to the Zoo (cross resistance)
2) Efivarenz (teratogen) and Nevirapine
3) RNA FoLD (N and F less important)
4) Raltegravir
Which non-invasive pathogens utilize "Lysogeny" in their pathogenesis and how?
1) Corynbacterium diptheria

- beta phage gives toxin gene without causing lysis
- low-iron conditions causes expression (repressor dissociates)

2) Vibrio cholerae
- pathogenicity island on CTX phage carries Type III secretion system, TCP, Cholera toxin, flagella and accessory enterotoxins

- ToxR, TcpP and ToxS activate ToxT, which activates promotor for Toxin and TCP
A patient presents with enlarged cervical LN and a gray pseudeomembrane in their throat.

What is the pathogenesis of the bug causing these symptoms?
This is C. diphtheria (non-invasive but can be absorbed)

Diagnose Clinically (like V. cholera!) and treat with anti-toxin

1) Aerosole droplets colonize nasopharynx or cutaneous cells (adhesin) and begin to produce toxin (low iron)

2) 1-7 d after see local necrosis and cause enlarged cervical

3) Gray adherent pseudomembrane forms in throat
A patient who recently returned from Peru presents with voluminous, painless and water diarrhea ("rice water"). The patients eyes are sunken.

What the pathogenesis of the bug causing these symptoms?
Non-invasive V. cholera (diagnose Clinically, but confirm with gram)

- motile, halotolerant, gram-negative rods

1) Estuary water consumption leads to colonization of intestine (TCP, LPS and capsule in O139)

**Flagella allow them to get through mucous to epithelial cells*

2) ToxR, ToxS and TcpP lead to ToxT expression, which leads to activation of the promotor for TCP and CTX.

3) CTX ADP-ribosylates Gs, leading to increase in cAMP and voluminous, painless discharge.
How do you treat the disease caused by the pathogen that leads to "rice water stool"?
ORS (Sodium and Glucose co-transport brings water back in to the body).

Cheap and Effective.

If Severe, give IV fluids
Which pathogens cross the placenta?
Which pathogen has 2-component regulatory systems and how does it work?
Salmonella (PhoP/PhoQ) (also B. pertussis with Bvgs/BvgA)

1) PhoQ senses low Mg inside phagosome and phosphorylates PhoP

2) PhoP upregulates pag genes (intracelllar) and represses prg genes (extracellular)

3) PhoP/PhoQ activity leads to PrmA/PrmB activity, that produces enzymes to alter LPOS to resist antimicrobial peptides.
Which pathogen has a Quorum Sensing Systems and how does it work?
Pseudomonas aeruginosa

1) When bacteria reach proper density, PAI (autoinducer) activates LASR (transcriptional regulator) to make Exotoxin A (inhibit protein synthesis).

2) LASR also activates PAI-2 (autoinducer), which activates RhIR (transcriptional regulator) to up-regulate VF1 and VF2
What pathogen exhibits cross-talk between Two-Component system and Quorum-Sensing?
Staph aureus

1) Autoinducer (AIP) from cell 1 binds AgrC (sensor) on cell 1, leading to transcription activation (AgrA) of toxins such as

- TSST-1
- Exfoliatoxin
- Alpha toxin

** This can happen from strain 1 to strain 2, but it be INHIBITORY **
A young women who recently traveled to India presents with abdominal cramps and "rose spots" on her abdomen.

What is the pathogenesis of the bug causing these symptoms?
Non-typhoid Salmonella (Zoonotic)

1) After ingestion, adhere to intestinal epitheium and M cells, and invade (Inv/Spa) by macropinocytosis

2) Remain in endosomes and translocate to the basal side, where they are released into lamina propria

3) Eaten by macrophages (survive with PhoP/PhoQ and PrmA/PrmB as wel as Spi/Ssa III secretion system)

4) In immunocompetent, inflammation by LPS causes GI symptoms
** In sickle cell or AIDS, it may disseminate causing septicemia and osteomyelitis
How does S. typhi pathogenesis differ from Non-typhoid salmonella?
Same until lamina propria

1) S. typhi (lead to peritonitis without treatment) disseminates from intestines to reticuloendothelial tissue and multiply

- 1-2 weeks late, they emerge in blood and bile, causing full-blown fever and septic shock and returning to intestine causing inflammatory response and hemorrhaging/perforation

2) Non-typhoid Salmonella enter macrophages in lamina propria (survives with PhoP/PhoQ and Spi/Ssa III secretion system).

-LPS causes inflammation and dissemination occurs in immunocompromised (AIDS and Sickle Cell)
How do you treat cases of Salmonella septicemia?

What is the difference between typhi and non-typhoid in terms of reservoir and virulent factors?
Remember, Typhi has Vi antigen and has only human reservoir, but Nontyphoid does NOT and is found in a lot of meat.

Don't always treat GI, but for Septicemia give antibiotics (Enterobacteria).
A 60 year old man presents with hemorrhagic lesions on his hips and in his mouth.

A Tzanck smear shows multi-nucleated giant cells

What is the viral life cycle of the bug causing these symptoms?
HSV-1 (60% orofascial) or 2 (60% genital)- Humans sole reservoir for transmission.

1) Attach to cell membrane with Heparin sulfate (gC and gB) ad HveA and C (gD).

2) Receptor-dependent fusion with gD, gB and gH

3) DNA replication (thymidine kinase and ribonucleotide reductase), Assembly and Egression

4) Latent infection as circular extrachromosomal episome in Neurons.

5) Reactivation with Stress, UV, trauma, ect (usually shorter and less severe except for HSK)
What pathogenic effects of HSV are observed?
1) Vesicular lesion formation (CPE), which is resolved by cell-mediated immunity

2) Viral shedding occurs in presence of high levels of neutralizing antibodies (Problem in Pregnancy and requires Cesarian section!)

3) Reactivation spread to CNS has 70% mortality if not treated

**reactivation is usually shorter and less severe, except for Herpetic Stromal Keratitis (HSK) with corneal opacity
How does the circular dsDNA virus that causes genital warts lead to oncogenesis? How is it treated?
HPV (Papovavirus)- Species and tissue specific replication

1) Upon viral integration (70% vs. 30% episomal), E1/E2 are down-regulated, and E6 (degrade p53) and E7 (binds and sequesters Rb) are up-regulated.

-Keratinocytes hypertrophy and neoplasia can ensue

2) Surgery is most effective, after Vaccination (quadrivalent or bivalent)
Which vaccines are live?
**Better immune response but more side effects **

1) MMR
2) Smallpox
3) BCG (TB)
4) Oral polio
Which vaccines are killed/inactivated?
**More doses with Ab response but less side effects**

1) Whole pertussis
2) Inactivated polio
3) Hep A
Which vaccines are Subunits?
** Repeated doses with adjuvant leading to Ab response **

1) Hep B
2) Tetanus
3) Diphtheria
4) Hib
5) Acellular pertussis (used more than whole killed)
What is a standard vaccine program for a child?
1) Hep B (3 doses between birth-18 months)- subunit
2) DTaP (3 doses in first 6 months, 15-18 months and 4-6 years- subunit)
3) Polio (3 doses in first 6 months and booster at 4-6 years-killed)
4) Hib (2-3 doses in first 6 months-subunit)
5) VZV (1 dose at 1-13 years-live)
6) MMR (1 dose at 12-18 months-live)
7) PCV (4 doses in first 15 months-killed)
8) Hep A (2 doses after 12 months-killed)
9) HPV (3 doses at ages 11-13)
10) Influenza (After 6 months of age)
What features define Bordetella pertussis vaccination and clinical manifestation?
Vaccine can be acellular (multiple subunits) or whole (inactivated but more side effects)

1) Gram-negative, fastidiously aerobic coccobacillus that causes tracheitis and bronchitis with mucus, cells and bacteria

2) Kids get it bad (life threatening with neurological sequele such as convulsions), but Adults (looks like a cold) are important reservoir

3) Early, mild stages are most infectious
What is the pathogenesis of B. pertussis?
Gram negative, fastidiously aerobic coccobacilli.

1) Enter trachea and bronchi by inhalation and attach to cilia of epithelium with filamentous hemagglutinin (FHA), pili and Pertussis toxin

2) Spread to LRT, leading to inflammation of the submucosa, cell destruction and persistent cough (can't clear material because escalator is impaired)

3) PT (A-B toxin) ADP-ribosylates Gi, leading to cAMP increase in host and

- Adenylate cyclase produced by B. pertussis as well

- Tracheal cytotoxin derived from peptidoglycan kills ciliated cells in escalator

- Heat labile toxin also damages epithelium
What virulence factors are associated with B. pertussis?
1) PT (A-B toxin) ADP-ribosylates Gi, leading to cAMP increase in host with disrupted cell signaling

2) Adenylate cyclase produced by B. pertussis as well

3) Tracheal cytotoxin derived from peptidoglycan kills ciliated cells in escalator

4) Heat-labile toxin also involved in tissue damage
How is transcriptional regulation of virulence gene expression achieved in B. pertussis?
Bvg two-component system (bvgA, bvgS). Like Salmonella

1) BvgS histidine kinase senses environmental signals (37 degrees or low Mg) and phosphorylates BvgA

2) BvgA is transcriptional activator of PT, fha genes, ect.
Supporting users have an ad free experience!