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Patho > 20. infectious pathology > Flashcards

20. infectious pathology Flashcards

1
Q

Sarcoidosis

A

is a systemic disease characterized by formation of noncaseating granulomas in different tissues and organs.
Classically seen in African American females
Aetiopathogenesis unknown

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2
Q

pathogenesis of sarcoidosis

A

likely due to disordered immune regulation, genetic predisposition and environmental triggers

↑CD4:CD8 T cells ratio

IL2 and IFNγ, and IL-8, TNF, macrophage inflammatory protein 1α (MIP1α)

Anergy to candida and PPD

Polyclonal hypergammaglobulinaemia

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2
Q

clinical presentation of sarcoidosis

A

bilateral lymphadenopathy
eye uvitis
skin erythema nodules
spelenomegaly

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3
Q

syndromes associated with sarcoidosis

A

lofgen syndrome
heerfordt syndrome
mikuliciz syndrome

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3
Q

lofgen syndrome

A

acute form of sarcoidosis
classic triad

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4
Q

heerfordt sydrome

A

LMN facial N. palsy
parotid gland enlargemnet
uveitis

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5
Q

mikuliciz syndrome

A

lacrimal and salivary gland enlargemnet

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6
Q

langhan giant cells with

A

schauman body
asteroid body

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7
Q

Diagnosis

A

Is a diagnosis of exclusion
Clinical and image finding
Biopsy- AFB, PAS
Kviem-Siltzbach test

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7
Q

Lab finding

A

Elevated serum ACE
Hypercalcemia (1- α hydroxylase activity of epithelioid histiocytes converts 25-dihydroxyvitamin D to 1,25-dihydroxyvitamin

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8
Q

Actinomycosis

A

is a rare, chronic and slowly progressive granulomatous disease
caused by filamentous, Gram-positive, anaerobic bacteria from the Actinomycetaceae family (genus Actinomyces) such as Actinomyces israelii

normal flora oral , gi , urogenitial

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8
Q

4 main types of actinomycosis

A

cervico facial - common
thoracic - like pnemonia at first
abdominal - appendix cecum and liver
pelvic - iud compli.

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9
Q

histology of actinomycosis

A

granules of gram postive bacteria

splendore heoppli rxn

yellow sulfur granules with sinus

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9
Q

Syphilis

A

Venereal disease which involves multiple systems (‘the great imitator’)
Caused by the spirochete Treponema pallidum

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10
Q

t. pallidum crcts

A

gram negative
obligate
spirochete
seen by dark field microscopy

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11
Q

histologic hallmark of syphyllis
how spirochetes attacks mechanism

A

obliterative endarteritis

bind to host fibronectin
type 4 hypersensitivity

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12
Q

stages of syphyllis

A

4
primary
secondary
latent
teritiary

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13
Q

primary

A

painless chancre

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14
Q

secondary

A

condyloma lata
rash (soles and mucosa)
lymphadenophaty

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15
Q

latent

A

asymptomatic

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16
Q

teritiary 3 manifestation

A

neurosyphillis
aortitis
gumma formation

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17
Q

neurosyphillis type

A

tabes dorsalis
meningovascular syphhilis
argyll roberston pupil

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18
Q

tabes dorsalis

A

affects dorsal column and dorsal spinal roots
leads to
loss of proprioception
high step page giat and
sensory ataxia

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19
Q

argyll robertson pupil

A

prostate pupil
dont constrict for light but does for objects

lesion of intercalates neurons in midbrain

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20
Q

aortitis and anerysm why

A

affects vasa vasorum

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21
Q

gumma formation in

A

liver hepar lobatum
skin
bone

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22
Q

congenital syphillis stages

A

early and late

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23
Q

early congenital syphilis

A

snuffles - rhinitis

hepatosplenomegaly

wimbers sign - bilateral destruction of tibial metaphysis

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24
Q

late syphilis

A

hutchinsons triad

hutchinson incisors

interstitial keratitis

sensorineural deafness

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25
Q

congenital common manifest

A

saddle nose
saber shin

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26
Q

Typhoid Fever
by

A

Caused by Gram-negative bacillus, Salmonella enterica serotype Typhi (formerly S. typhi).
S. enterica serotypes Paratyphi A, B, or C, can cause a similar illness
Humans are the only reservoir for Salmonella enterica serotype Typhi
IP 7-14 days on average

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27
Q

salmonella typhi antigens

A

H antigen - flagellar
O antigen - somatic
Vi antigen - LPS

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28
Q

pathogenesis

A

The bacteria multiply by attaching to microvilli of the intestinal surface (M cells)  perforate through the intestinal wall and are phagocytosed by macrophages

 S. typhi alters its structure to resist destruction and allows it to exist within the macrophage
(faculitative intracellular )

 Bacterial multiplication in Mononuclear Phagocytic system

spread via lymphatics to get access to reticuloendothelial system and then disseminate throughout the body.

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29
Q

Morphology of organs

A

Peyer’s patches enlargement
Superficial longitudinal mucosal ulcers aligned along Peyer’s patches
Lymphadenopathy
Hepatospleenomegaly

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30
Q

Sign and symptom

A

Constipation or mild diarrhea
Stepwise fever
Relative bradycardia (pulse-temperature)
Headache, fatigue, malaise, loss of appetite, cough, Skin rash or rose spots
Hepatosplenomegaly(HSM)

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31
Q

Neurologic manifestations

A

“Typhoid encephalopathy”: altered consciousness, delirium, and confusion.
Acute psychosis
Meningeal signs

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32
Q

Neurologic manifestations tests

A

kernig and brudzinski

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33
Q

Diagnosis

A

CBC: Leukopenia with relative lymphocytosis. Rarely thrombocytopenia

Serologic test-
-Widal test ( agglutinating antibodies against O-somatic and H-flagellar antigens) is positive after the first week.
False positive; cross reactivity with other bacteria, vaccination, and endemic areas.

-Rising titer is more important and a value 1:160 is convincing

-‘Typhidot’ is a rapid test used to diagnose typhoid fever, and is negative in the first week and positive thereafter.

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34
Q

Complication

A

Intestinal haemorrhage and perforation (5% and in 3rd week)
Metastatic abscesses in other organs
Osteomyelitis (sickle cell disease), endocarditis, glomerulonephritis, meningitis , encephalitis etc..

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35
Q

chronic carriers how

A

Chronic typhoid fever (3-5%): Gall bladder (stones)or renal diseases predispose to carrier. Vi antigens for S.typhi is used to screen the carrier.
Relapse (10-20%)

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36
Q

Schistosomiasis

A

Acute and chronic parasitic disease caused by blood flukes of the genus Schistosoma

also called bilharziais

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37
Q

types of schistosoma species

A

s. hematobium - urogenital

s. mansoni
s. japonicum
s. mekongi
s. intercallatum - intestinal liver

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38
Q

life cycle

A
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39
Q

where do schistosomas mature

A

potal vasculature

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40
Q

male and female pair by

A

BATT

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41
Q

pathogensis

A

due to host inflammatory reactions

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42
Q

acute schistosoma cytokines

A

TNF a
IFN y
IL 1
IL6
IL12

More Th1

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43
Q

Chronic schistosoma cytokines

A

IL4
IL5
IL10
IL13
More Th 2

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44
Q

clinical feature of acute schistosoma (Katayamas syndrome)

A

fever
abdominal pain
diarhea
cough
RES enlargement

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45
Q

clinical features of chronic schistosoma

A

egg deposit in tissue
inflammation
repair by fibrosis

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45
Q

instestinal schistosoma characteristic

A

Patches or polyps
Fibrosis and obstruction
Granuloma around the egg
Present with chronic bloody diarrhea and abdominal pain

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45
Q

liver schistososma plus main feature

A

Reason for most deaths

Perisinusoidal and periportal fibrosis (Symmers’ pipe stem fibrosis)

Portal hypertension  HSM, esophageal varices, ascites etc…

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46
Q

lung schistosoma

A

In patients with portal hypertension
Eggs pass through portocaval
anastomosis
Granulomatous pulmonary arteritis
Pulmonary hypertention
Rt. Sided heart failure (Cor pulmonale)

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46
Q

Urinary schistosoma

A

Ureteric obstruction  obstructive uropathy
Squamous metaplasia  squamous cell carcinoma
Bladder calcification
Recurrent gross hematuria “men menstruation”
Membranoproliferative glomerulonephritis (MPGN) and/or membranous nephropathy

47
Q

Genital schistosomiasis

A

Reported in endemic areas
Usualy caused by S. hematobium fallopian tube involvment Ectopic pregnancy and placenta rarely described
Sandy patch/rice grain (most common), Polyps /nodules / Ulcers

48
Q

Neuroschistosomiasis

A

Most frequently due to embolization of eggs, but some cases of adult schistosomes traveling to the CNS vasculature have been reported.
S. japonicum primarily involves the brain, while S. mansoni and S. haematobium primarily affect the spinal cord. However, occasional cases of cerebral schistosomiasis due to S. mansoni continue to be reported

49
Q

Amoebiasis

A

Protozoal disease by genus Entamoeba hystolytica (lytic action on tissues by protase and ionophore)
Feco oral transmission (poor sanitation)
No animal reservoir
It is endemic in Ethiopia
The two common species of intestinal Entamoeba with identical morphology are E. histolytica and E. dispar (nonpathogenic)

50
Q

Amoeba proteins involved in tissue invasion

A

Cysteine proteases, which lyse proteins of extracellular matrix.
Lectins on parasite surface that bind to carbohydrates on colonic epithelium and RBCs.
Channel forming proteins that contains an ameba pore that makes pores in plasma membrane and lyses it

51
Q

The parasite occurs in 2 forms

A

Trophozoite: active adult form, in the tissues and diarrhoeal stools, and PAS+, fail to survive outside and destroyed by gastric secretions.
Cyst: infective stage, Four nuclei, formed stools but not in the tissues.
Transform to trophozoite in the intestine

52
Q

Clinical features

A

Most infections are asymptomatic
Abdominal pain
Bloody and mucoid diarrhea
Malaise
Other presentations: amoebic liver abscess, and ameboma (tender abdominal mass)

53
Q

Amoebic colitis

A

Most common type of amoebic infection
Caecum > ascending colon > sigmoid > rectum > appendix
Begins as a small area of necrosis of mucosa which may ulcerate
Flask-shaped ulcers = Undermining ulcer
Margin of the ulcer shows trophozoites + acute on chronic inflammation

54
Q

Amoeboma

A

Napkin-like constrictive lesion
Inflammatory thickening of the wall of colon
Intestinal obstruction
Ddx: carcinoma of the colon.
Mic: granulation tissue, fibrosis and clusters of trophozoites

55
Q

Extraintestinal Amebiasis

A

Peritonitis by perforation of amoebic ulcer of colon,
Lungs and pleura by rupture of amoebic liver abscess or hematogenous
Haematogenous spread to cause amoebic carditis and cerebral lesions
Skin ulcer: Perianal, Vulvar and Penile

55
Q

Amoebic liver abscess

A

40% patients
From peritoneum or portal venous drainage
Amoebic liver abscess may be single or multiple
Multiple zones of liver necrosis  confluence  ‘liver abscess’ (not true abscess: no neutrophils in or around the cavity)
Fever and RUQ abdominal pain

55
Q

Hydatid Disease

A

It is caused by ingestion of eggs of echinoccal species shed by dogs or foxes.
Humans are accidental intermediate hosts

56
Q

pathogenesis of haydatid disease

A

Eggs hatch in the duodenum and the larvae penetrate the intestine and disseminate haematogenously  the larvae lodge within the capillaries Many such larvae undergo encystation
~2/3 of human E. granulosus cysts are found in the liver, 5–15% in the lung, and the rest in bones and brain or other organs.

56
Q

Species of echnococal

A

Three out of four known species are of medical importance in humans.
Echinococcus granulosus: the most common, causes cystic echinococcosis
Echinococcus multilocularis: rare but is the most virulent, causes alveolar echinococcosis)
Echinococcus vogeli: the rarest

57
Q

Morphology of E.granulosus

A

Unilocular cyst (>10 cmØ/ >5yr)

Enclosing an opalescent fluid

Inner , nucleated, germinative layer and an outer, opaque, non-nucleated layer with delicate laminations.

Outside this opaque layer, there is a host inflammatory reaction that produces a zone of fibroblasts, giant cells, and mononuclear and eosinophilic cells.

In time a dense fibrous capsule forms.

In time, daughter cysts develops.

57
Q

Degenerating scolices of the worm produce a fine, sandlike sediment within the hydatid fluid

A

(hydatid sand).

57
Q

Complications

A

Rupture
Anaphylaxis
Dissemination
Infection
Recurrence

58
Q

Onchocerciasis

A

= River blindness
Caused by a filarial nematode Onchocerca volvulus
leading cause of preventable blindness in sub-Saharan Africa
Affects 17 million people in Africa, South America, and Yemen
Onchocerciasis is endemic in SNNPR, Amhara, Beneshangul-Gumuz and Oromia regions

59
Q

life cycle or pathogeneiss

A

Bite of a blackfly introduce third-stage larvae into the human skin, which mature into adult parasites (macrofilariae) over 6-12 months  In the skin inseminated females produce microfilariae  disseminate to the eye chambers

60
Q

skin manifestations

A

Leopard, lizard, or elephant skin: chronic, itchy dermatitis with focal hyper or hypopigmentation and scaling
Onchocercoma is subcutaneous nodule over bony prominences of adult O. volvulus parasites and body response.

61
Q

eye manifestations

A

Eosinophilic infiltrate against degenerating microfilariae
Punctate keratitis sclerosing keratitis
Anterior chamber inflammation, iridocyclitis and glaucoma
Choroid and retina: atrophy and loss of vision

62
Q

mazzotti rxn

A

Mazzotti reaction accentuated keratitis by antifilarial drugs

63
Q

Toxoplasmosis

A

Infection caused by protozoa, T.gondii

63
Q

T gondii exists in 3 forms

A

oocyst
bradyzoits
tachyzoits

64
Q

life cycle

A

from cat feces oocyst or tissue cysts

ingested then tachyzoit

localize as bradyzoit

65
Q

transmission

A

ingestion
vertical
horizontal .. blood transfusion

66
Q

hosts type

A

The cat is the only definitive host, Intermediate hosts (birds, rodents) and humans are a dead-end host.

67
Q

T. gondii forms a ………….. protected from lysosomal fusion.

A

parasitophorous vacuole (PV)

68
Q

Acute acquired Toxoplasmosis

A

10 - 20%
Focal inflammation
Myocarditis, encephalitis, splenomegaly, lymphadenitis
Recovery with in few weeks to months
latent infection

69
Q

chronic toxsoplasmosis:

A

schizophrenia and other neurologic conditions, hypothesized but studies are inconclusive

70
Q

Congenital toxoplasmosis plus types

A

Seen in primary infection of mother
early and late

71
Q

tourch group

A

TORCH group (toxoplasmosis and others [syphilis, tuberculosis, listeriosis], rubella, cytomegalovirus, herpes simplex)

72
Q

Early infection:

A

low transmission, but severe disease (abortion/stillbirth and/or sever malformation)

73
Q

Late infection:

A

high transmission, more benign symptoms

73
Q

presentation time

A

Delayed presentation peaks is in second or third decade, most commonly bilateral chorioretinitis

74
Q

congenital toxo triad

A

chi
chorioretinitis
intracranial calcification
hydrocephalus

74
Q

Leishmaniasis

A

Caused by an obligate intracellular kinetoplastid protozoan parasites

75
Q

Life cycle involves two forms:

A

Promastigotes in the sand fly vector and
Amastigote in the host macrophages.

76
Q

in anergic hosts

A

Anergic host: dominant Th2 cytokines such as IL-4, IL-13, and IL-10  inhibiting the microbicidal activity of macrophages  diffuse lesion

76
Q

leshmania evasion

A

Promastigotes produce Lipophosphoglycan and gp63

Amastigotes express a proton-transporting ATPase, which maintains the phagolysosome pH at 6.5 (n=pH of 4.5).

76
Q

Host immune reaction

A

-CMI - Th1- INF Y
leshamania impair Th1

↑ production of hepcidin (iron exporter)
↑ ferritin (binds free iron)
↓ macrophages transferrin receptor and
↑ removal of iron from the phagosome

77
Q

Lipophosphoglycan

A

activates complement (leading to C3b deposition on the parasite surface) and inhibits complement action (preventing MAC insertion into the parasite membrane).

78
Q

gp63

A

Gp63 is proteinase againest complement and some lysosomal enzymes. Gp63 also promotes promastigote adhesion to macrophages.

79
Q

Four different types in humans

A
80
Q

Visceral Leishmaniasis

A

Species: L. donovani, L. chagasi, L. infantum

81
Q

Cutaneous leishmaniasis

A

L. major, L. aethiopica

Papule surrounded by induration  shallow and slowly expanding ulcer  usually heals by involution within 6 to 18 months without treatment

82
Q

Mucocutaneous leishmaniasis

A

L. braziliensis

83
Q

Diffuse cutaneous leishmaniasis

A

L. aethiopica

Single skin nodule  generalized skin nodule

84
Q

Diagnosis of Leishmaniasis
and test

A

Cytology/histology
Splenic aspirate: it is the preferred specimen, highest yield and Sn of 93-99%
Bone aspirate: Sn 53-86%
Lymph node aspirate: Sn 53-65%
Skin/mucosa FNAC/biopsy
Leishmanin skin test (Montenegro skin test)

85
Q

Malaria

A

Malaria is a protozoal disease caused by species of plasmodia

86
Q

transmission

A

Transmision: through bite of female Anopheles mosquitoes, blood transfusion and transplacental

87
Q

2 types of malaria

A
88
Q

Benign malaria

A

P. vivax, P. ovale, P. knowlesi, and P. malariae
low levels of parasitemia
Mild anemia
Rarely splenic rupture and nephrotic syndrome.

89
Q

Malignant malaria

A

P. falciparum
High levels of parasitemia
Severe anemia
Cerebral symptoms
Renal failure
Pulmonary edema
Death

90
Q

2 stages of malaria

A

exoerythrocyte stage
erythrocyte stage

91
Q

exoerythrocyte stage

A

asymtomatic

sporozoite by thrombospondin to hepatocytes

92
Q

in hepatocyte different species

A

P. vivax and P. ovale form latent hypnozoites in
hepatocytes, which cause relapses of malaria weeks to months after initial infection

other to merozoitas

93
Q

erythrocyte stage 3 phases detail

A

1 merozoit look like a ring

2 late throphozoit

3 digest hg called schizont

94
Q

Features of P. falciparum account for its severity

A

P. falciparum infect RBC of any age
RBC rosette
RBC sequestration;

P. falciparum erythrocyte membrane protein 1 (PfEMP1) on RBCs binds to ligands on endothelial cells(CD36, thrombospondin, VCAM-1, ICAM-1, and E-selectin)

Red cell sequestration blocks blood flow ↓tissue perfusion  ischemia

95
Q

kidneys malaria

A

Nephrotoxic (pigment) ATN “blackwater fever”
P. falcipurum= Proliferative glumerulonephritis
P. malarie = Membranous glumerulonephritis

96
Q

Tropical Splenomegaly Syndrome
(Hyperreactive malarial syndrome (HMS))

A

Exaggerated immune response to recurrent or persistent malarial infection
IgM aggregates are phagocytosed by the cells of the RES, stimulating macrophage and T-cell hyperplasia
Chronic abdominal swelling (64%) and pain (52%)

97
Q

Cerebral malaria
nodule called

A

The major cause of death in children with malaria.
Unconsciousness, focal neurological symptoms and coma
Malaria of non immunes
Petechial hemorrhage in subcortical white mater
Degeneration of neurons
Demyelination and pericapillary ring hemorrhage.

Microglial nodule called “Durck’s granuloma” (“malarial granuloma”)

98
Q

kind of lymphoma

A

↑endemic Burkitt’s lymphoma (eBL) in malaria endemic area

99
Q

Tenia versicolor/ Pityriasis Versicolor (PV)
by
risk factors
pathogenesis
under microsope koh

A

Malassezia furfur (normal skin flora)

Risk factors include sweating and oily skin

Pathogenesis. Malassezia changes from a yeast to hyphaI form under the influence of predisposing factors. Produces dicarboxylic acid, which inhibits tyrosinase in epidermal melanocytes

spaheti meatball

100
Q

Dermatophytoses
by

A

Superficial fungal infections usually affect all parts of the skin
The commoan dermatophytes include Microsporum, Trichophyton, and Epidermophyton.

101
Q

Candidiasis
by
3 clinical form
under micro koh

A

C. albicans is present as normal flora of the skin, mouth, vagina and gastrointestinal tract.

thrush
hyperplasia
erythematous

braching budding

102
Q

Mycetoma
common name

A

Classified as a Eumycetoma (fungal disease) or Actinomycetoma

Usually acquired while performing agricultural work

madura foot

103
Q

Aspergillosis
by
predisposing factors

A

Aspergillus fumigatus is the most common pathogenic species of the fungus

neurtopenia
corticosteriod

104
Q

2 type of aspergilloma

A

colonizing
invasive

105
Q

Monod’s sign

A
106
Q

Mucormycosis (Zygomycosis)

A

Major predisposing factors are neutropenia, corticosteroid use, DM with ketosis, iron overload, and breakdown of the cutaneous barrier
Most patients are Primarily affect nasal turbinates leading to sinusitis, orbital inflammation with proptosis and menigioencephalitis (rhinocerebral mucormycosis)
Has propensity to invade blood vessel causing cavernous sinus thrombosis and pituitary infarction

black fungus

107
Q

Histoplasmosis

A

Infects humans by inhaling spores present in soil contaminated from chicken faeces.

Causes enlarged lymphoreticular tissue and destroying adrenal (Addison’s disease)

intracelular

108
Q

Coccidioidomycosis

A

Infection is acquired by inhalation of the spores of coccidioides immitis
Patients develop delayed type of hypersensitivity reaction to the fungus
Have high rate of infectivity (spores ingested by alveolar macrophages block fusion of the phagosome and lysosome )

109
Q

Cryptococcosis

A

C. neoformans in pigeon dropping

In immunocompetent
Focal or diffuse lung lesion: chronic granuloma and mucoid type of pneumonia

In immunosuppressed
meningoencephalitis (typically gelatinous meningitis) and disseminated cryptococcosis

110
Q

Measles (ኩፍኝ)

A

Caused by an ssRNA virus of the paramyxovirus family (Rubeola virus)

111
Q

spread by

A

Spreads by respiratory droplets multiplies within upper respiratory epithelial cells (via receptors, mainly, CD46 and SLAM) spreads by blood throughout the body replicate in T lymphocytes, macrophages and dendritic cells.

112
Q

manifestations 5

A

conjuctivitis
lymphadenopathy
kopliks spot
exanthem
warthin finkeldey cell giant cells

113
Q

Herpes Simplex Infection

A

HSV-1 oral cavity and HSV-2 genitals

Reactivation associated with trauma, URTI, pregnancy menstruation, UV light, immunosuppression

114
Q

hallmark for HSV\
and 3 M for HSV

A

hallmark of HSV infection is large pink-to-purple intranuclear (Cowdry type A) inclusions, which push nuclear chromatin to periphery

MARGINATION OF CHROMATIN
MOLDING
MULTINUCLEATED GIANT CELL

115
Q

Varicella Zoster virus (VZV)

A

Causes varicella (chickenpox (ጉድፍ)) and zoster (shingles).
Varicella is usually a disease of children.
Centrifugal: trunk to face and extremities
Dormancy occur in trigeminal and dorsal (sensory) root ganglia.
Reactivation can cause zoster (shingles) with 15% to 20% complaining postherpetic neuralgias

116
Q

Morphology of infectious mononucleosis

A

EBV
kissing disease

Peripheral blood lymphocytosis (>60% of WBC are atypical T-cells )
Lymphnodes: paracortical zone expansion and B cell proliferation (atypical)
Splenomegaly
Hepatomegaly and Hepatitis
Meningitis and Encephalitis
Pneumonia

Patho (33 decks)

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