Cryptosporidium exhibits a monoxenous lifecycle and affects both humans and animals. Infected domestic animals are reservoirs for susceptible humans. in the lifecycle of the cryptosporidium, Thin-wall oocyst (used for autoinfection) and Thick wall oocyst are (thrown into the environment for infecting another host). Invaginate cell membrane and forming #bi-layered membranous vacuole (parasitophorous vacuolar membrane) creates a conducive environment for the parasite for escaping the host immune system.

1. By Dr. Fentahun Wondmnew
College of Veterinary
Medicine

3. Recognized in mice in 1907
Reported in humans in 1976
Recognized globally in
1980s and 1990s
Ernest Edward Tyzzer
History

4. Protozoan
Phylum:
Apicomplexa
Class: Sporozoasida
Order: Eucoccidiida
Family
Cryptosporiidae
Genus:
Criptosporidium
Species >20
C. Parvum
C. hominis
 C. andersoni
 C. bovis
 C. muris
C. meleagridis
 C. felis, etc.
>44 genotypes
Etiology

5. Occurrence
 Worldwide
 Cryptosporidiosis
kills more than 2
million people in
developing world
 Prevalence of C.
parvum in preweaned
calves ~50
 Young calves has
more zoonotic risk
Hosts
 Animals
 Cattle
 Lambs
 goat kids
 foals
 piglets
 Human
 All classes of vertebrates
.
EPIDEMIOLOGY
.

6. Source of Infection and Transmission
Transmission
 Directly from calf to calf
 Indirectly via fomite or
human transmission
 Person to person
 Fecal contamination of
environment, feed or
water supplies
 Recreational water use,
such as in pools and
lakes
source of infection
 Faeces with oocysts
Small number of oocysts
(as low as one) are
required for infection
Large numbers of
oocysts are excreted
during patency in calves

7. Risk Factors
Predisposing factors are not well
understood
Young are more affected
Concurrent enteric infections particularly
rotavirus and coronavirus worsen it
Immunologically compromised animals
Case–fatality rates are low and self-limiting
Animal handlers on cattle farms can be at
high risk

8. Zoonotic Implications
Zoonotic and recently emerged
Infected domestic animals are reservoir for
susceptible humans
 In immunocompetent patients, diarrhea
and rapid weight loss but self limiting
Symptoms lasts 3 to 12 days
In immunologically compromised persons,
clinical disease may be severe particularly in
AIDS patients

9. Lifecycle
Cryptosporidium exhibits a monoxenous
(single-host) life cyle
Infection begins by ingestion of oocysts
excystation in the gut forms infect epithelial
cells and Type I meront formed (Asexual
reproduction)
Merozoits gives Type II meronts (Sexual
reproduction)

10. Lifecycle contd
Merozoitses forms undiffferentiated gamonts
These gives male(Microgamonts) and
female(macrogamonts )
A mating of male and female gamonts gives rise
to Zygote
 A zygote produces :
 Thin wall oocyst (used for auto infection)
 Thick wall oocyst (thrown to environment for infecting another
host)

11. Life cycle contd.
In auto infection part (thin oocyst) develops into the
Sporozoit
This grows into Trophozoite (which infect enterocyt
and continue the life cycle for chronic infection)

12. Life cycle contd.

13. PATHOGENESIS
Sporulated oocyst ingested by the host
Exocysts intestine or stomach
Each motile sporozoite migrates and penetrates the
cell
Invaginate cell membrane and form #bi-layered
membranous vacule (parasitophorous vacuolar
membrane)
 outer layer is host derived
 inner layer is parasite derived
In the cell sporozoite develops into a trophozoite
Undergoes asexual reproduction (schizogony or
merogony) and produce type 1 meronts (schizonts)

14. Parasitophorous Vacuolar Membrane

15. PATHOGENESIS contd.
Parasitophorous vacuolar membrane
The host-derived outer layer of the vacuole
disintegrates
The inner PVM thickens and acts as the
interface between the developing parasite
and the host cytoplasm
This keeps the parasite being located
intracellularly to be external to the cell
cytoplasm (i.e., extracytoplasmic).

16. PATHOGENESIS contd.
Types 1 meronts containing 16 merozoites,
are released from the enterocyte
Each merozoite infects a new enterocyte
Replicates and develops into new type 1
meronts to repeat the cycle
ENTER into reproductive phase, replicate
and develop into a type 2 meront, each
contains four merozoites

17. PATHOGENESIS contd.
Finally two types of oocyst are
produced and slough off the epithelial
layer.
The thin-walled oocysts (~20% of the
overall population of oocysts) remain
in the alimentary tract and sustain an
autoinfection
Thick-walled oocysts (~80%) are
passed in the feces

18. PATHOGENESIS contd.
Zoites infect vicinal enterocytes and endogenous
forms spread to the enterocytes of both the villi and
crypts
This leads to:
Disrupt the microvillous border, which leads to the
loss of mature enterocytes
Loss of membrane-bound digestive enzymes
Diminishes the absorptive capacity of the intestine
Reduces the uptake of fluids, electrolytes, and
nutrients from the intestinal lumen

19. PATHOGENESIS contd.
This leads to:
disrupt the microvillous border, which leads
to the loss of mature enterocytes
Loss of membrane-bound digestive
enzymes
Diminishes the absorptive capacity of the
intestine
Reduces the uptake of fluids, electrolytes,
and nutrients from the intestinal lumen

20. PATHOGENESIS contd.
Alters osmotic pressure
 Atrophy of intestinal villi
Alters uptake of fluids, electrolytes,
and nutrients
Malabsorption syndrome

21. CLINICAL FINDINGS
Human
 Diarrhea
 Stomach cramps
 Dehydration
 Nausea
 Vomiting
 Fever
 Weight loss
 Sometimes no
symptoms are seen
Animals
 No pathognomonic sign
 Mild to moderate diarrhea
in calfs 5 to 15 days old
 Yellow, pale, watery and
mucus containing feces
 In most cases, diarrhea is
self-limiting
 Recovery can occur
between 6 and 10 days after
the onset of diarrhea

22. Prevention and control
Maintenance of a clean environment
Effective management strategies
Removing neonates from the dam within 1 hour of
birth
Disinfectants farm with ammonia-based or hydrogen
peroxide containing disinfectants

23. Treatment Options
Immunotherapeutic
colostrum is unlikely to be effective
Oocyst-based vaccine of C. parvum (gamma
irradiated) has a protective response in
calves
Antigens derived from oocysts appear to be
promising immunogens

24. Treatment Options contd.
Chemotherapy
Has limited success
Quinones, aminoglycosides and folate
antagonists have mixed success
Paromomycin sulfate orally daily for 11
consecutive days from the second day of age
in goat kids has a little preventive effect for
diarrhea
 Supportive Oral or intravenous rehydration

25. Immunity against cryptosporidium
Infection may result in a serum antibody response, but
both cell-mediated and humoral responses are
important in immunity against cryptosporidia
together with innate immunity.

26. Interferon-c and natural killer (NK) cells in
innate immunity
 IFN-c elicits an intracellular signaling cascade in the
epithelial cells and enhances inflammatory responses.
Then Macrophages produce free radicals of nitric
oxide (NO) and C. parvum will be attacked
NK cells kill intra cellular C. parvum by defusing toxic
intracellular proteins ( perforin and granzyme) into
the cells.
Dendritic cells contribute host immune response
against C. parvum, by activating innate immune
mechanisms

27. Complement system
There are three pathways
1. Classical pathway: antigen antibody reaction
2. Bacterial endotoxin pathway: alternative pathway
3. Lectin pathway –manos binding lectin
 C. parvum can activate both, the classical and lectin
pathways, leading to the deposition of C3b on the parasite
 This triggers opsonization which facilitate phagocytic
removal of C. parvum
 The role of complement in immunity to C. parvum is only
apparent when other parts of the specific immune response
are weakened as seen in AIDS

28. Adaptive immunity
A study showed the importance of T-lymphocytes but
not that of B-lymphocytes in cryptosporidium
removing process
Helper T cells attack the parasite by activating the
macrophage, dendritic cell and Tc cells

29. Adaptive immunity contd.
Th1 cells secrete IFN-c and TNF-a, which make
epithelial cells effective in protecting against
intracellular infections.
Th2 cells secrete IL-4, IL-5, IL-10 and IL-13, which
activate B-cells to upregulate antibody production
Whereas
no data exist that support the involvement of CD4+ T-
cells